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

{“questions”:{“di61c”:{“id”:”di61c”,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Authors: Amy Babb, MD – Vanderbilt University and Kaitlin M. Flannery, MD, MPH – Stanford University \r\nA 16-year-old girl with a history of orthotopic heart transplantation is admitted with one week of nausea, vomiting, and fatigue. She is scheduled for an urgent endomyocardial biopsy due to suspected rejection. Past medical history includes stage 3 chronic kidney disease and type 2 diabetes, and current medications are aspirin, atorvastatin, carvedilol and empagliflozin. Which of the following laboratory values is MOST likely to be associated with euglycemic diabetic ketoacidosis associated with empagliflozin?\r\n”,”desc”:”EXPLANATION \r\nEmpagliflozin, dapagliflozin, canagliflozin, and ertugliflozin are sodium-glucose cotransporter-2 (SGLT2) inhibitors used for managing type 2 diabetes, chronic kidney disease, and heart failure. SGLT2 inhibitors work by blocking reabsorption of glucose and sodium in the proximal renal tubules leading to glucosuria, natriuresis, and diuresis. Adult studies and limited pediatric studies have shown SGLT2 inhibitors can decrease HbA1c, proteinuria, brain natriuretic peptide (BNP), and blood pressure, and modestly improve ejection fraction in heart failure. Adverse effects include urinary tract infection and fungal genital infections (due to glucosuria), headache, diarrhea, vomiting, and euglycemic diabetic ketoacidosis (eDKA). \r\n\r\nThe mechanism of SGLT2-associated eDKA is not completely understood. However, diagnostic criteria of eDKA are similar to classic DKA. The most notable difference is the absence of hyperglycemia in eDKA that is typically seen in classic DKA. DKA occurs during a relative or absolute state of insulin deficiency with increased counter-regulatory hormones, including glucagon, corticosteroids and catecholamines. The imbalance of hormones leads to ketone formation and anion-gap metabolic acidosis. In the presence of SGLT2 inhibitors, glucosuria and diuretic effect lowers the serum glucose and decreases the overall insulin requirement. During periods of stress, such as illness, nausea, vomiting, fasting and surgery, the low insulin\/high glucagon environment can lead to eDKA (see Figure 1 below). \r\n\r\n \r\n \r\n \r\nFigure 1. Proposed role of sodium-glucose cotransporter 2 (SGLT2) inhibition in euglycemic diabetic ketoacidosis (eDKA). Classic DKA results from insulin deficiency (absolute or relative) and concurrent increase in counter-regulatory hormones leading to ketosis, hyperglycemia, and osmotic diuresis. In contrast, SGLT2 inhibitor therapy in a well-compensated individual at baseline causes glucosuria, mild volume depletion, and lower serum glucose levels, associated with decreased insulin secretion. During times of intercurrent illness and\/or metabolic stress, such as surgery or gastrointestinal illness, decreased carbohydrate intake coupled with lower serum glucose levels can further depress insulin secretion. This can ultimately lead to eDKA (red box). \u2217Possible pathways of carbohydrate deficiency and causes of insulinopenia. Abbreviations: BP, blood pressure; PO, oral. (From: Wang KM and Isom RT. SGLT2 inhibitor-induced euglycemic diabetic ketoacidosis: A case report. Kidney Med. 2020;2:218-221. Used under Creative Commons License.) \r\n\r\nA diagnosis of eDKA requires the following: \r\n1.\tBlood glucose < 200 mg\/dL\r\n2.\tKetonemia (serum beta-hydroxybutyrate greater than 3 mmol\/L) \r\n3.\tAnion gap metabolic acidosis: \r\na.\tArterial pH < 7.3 \r\nb.\tSerum bicarbonate < 18 mEq\/L \r\nc.\tAnion gap > 10 mmol\/L \r\n\r\n\r\nTreatment of eDKA includes initiation of IV insulin infusion and dextrose solution, as well as IV fluid repletion and electrolyte management. The goal of therapy in eDKA is not to lower the serum glucose, but to replenish the insulin stores necessary to reduce ketone production. Monitoring of urine glucose can help determine residual SGLT2 inhibitor activity, and urine\/serum ketones can guide efficacy of treatment. \r\n\r\nDue to the frequency of reported perioperative eDKA events, the FDA updated its safety labeling in 2020 to recommend that empagliflozin, dapagliflozin, and canagliflozin be held for THREE days and ertugliflozin for FOUR days prior to elective procedures. In addition, a recent study from Massachusetts General Hospital has shown that anion gap metabolic acidosis develops in all patients when SGLT2 inhibitors were not held appropriately. \r\n\r\nWhen patients on SGLT2 inhibitors present for urgent\/emergent procedures, they must be monitored closely for the development of eDKA. Signs and symptoms of eDKA are non-specific and include nausea, vomiting, abdominal pain, fatigue, tachycardia, and tachypnea. Unfortunately, these are also signs of orthotopic heart transplant rejection and heart failure. \r\n\r\nDue to increased evidence in the literature, candidacy and indications for SGLT2 inhibitor use are being expanded to include children ages ten years and older, non-diabetic patients with heart failure and congenital heart disease patients. This trend will increase the likelihood of pediatric cardiac anesthesiologists and pediatric anesthesiologists managing patients treated with SGLT2 inhibitors in the perioperative setting.\r\n\r\nThe correct answer is B. EDKA is characterized by the finding of increased serum and urine ketones, such as serum beta-hydroxybutyrate 5, in the presence of an increased anion-gap metabolic acidosis and relatively normal serum glucose levels. \r\n\r\n \r\nREFERENCES \r\nGrube PM, Beckett RD. Clinical studies of dapagliflozin in pediatric patients: a rapid review. Ann Pediatr Endocrinol Metab<\/em>. 2022;27:265-72.\r\n\r\nSteinhorn B, Wiener-Kronish J. Dose-dependent relationship between SGLT2 inhibitor hold time and risk from postoperative anion gap acidosis: a single-centre retrospective analysis. Br J Anaesth<\/em>. 2023 Oct;131(4):682-6.\r\n\r\nChow E, Clement S, Garg R. Euglycemic diabetic ketoacidosis in the era of SGLT-2 inhibitors. BMJ Open Diab Res Care<\/em>. 2023;11:e003666.\r\n\r\nFDA revises labels of SGLT2 inhibitors for diabetes to include warnings about too much acid in the blood and serious urinary tract infections (fda.gov). 2022. Available at: https:\/\/www.fda.gov\/drugs\/drug-safety-and-availability\/fda-revises-labels-sglt2-inhibitors-diabetes-include-warnings-about-too-much-acid-blood-and-serious. Accessed 7\/17\/2023.\r\n\r\n”,”hint”:””,”answers”:{“qqk3f”:{“id”:”qqk3f”,”image”:””,”imageId”:””,”title”:”A.\tArterial pH 7.35″},”un9x4″:{“id”:”un9x4″,”image”:””,”imageId”:””,”title”:”B.\tSerum beta-hydroxybutyrate 5 mmol\/L “,”isCorrect”:”1″},”gxnjc”:{“id”:”gxnjc”,”image”:””,”imageId”:””,”title”:”C.\tBlood Glucose 350 mg\/dL”}}}}}

{“questions”:{“nalqn”:{“id”:”nalqn”,”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 14-year-old girl with a past medical history of obesity and family history of Factor V Leiden presents with chest pain, dyspnea, tachycardia and hypotension. Computed tomography pulmonary angiography demonstrates a pulmonary embolism in the main pulmonary artery with extension into bilateral branch pulmonary arteries. Transthoracic echocardiography reveals interventricular septal flattening, severe tricuspid regurgitation, and severely diminished right ventricular function. Which of the following medication regimens is the MOST appropriate treatment for severe high-risk pulmonary embolism?”,”desc”:”EXPLANATION \r\nThough less common in children than adults, pulmonary embolism (PE) is associated with significant morbidity and mortality. Guidelines for management of acute pulmonary embolism in children are based on those created for adults, due to the more established literature in this population. In most guidelines, risk stratification of pulmonary embolism is the initial step in the diagnostic and treatment algorithm. High risk (massive) pulmonary embolism is typically defined as having signs of severe cardiopulmonary dysfunction or obstructive shock, such as tachycardia, hypotension, and altered mental status. Intermediate risk (sub massive) PE typically lacks signs of obstructive shock but retains the signs of right ventricular (RV) strain as evidenced by echocardiography and electrocardiogram, or elevated cardiac enzymes. \r\n\r\n\r\nSigns and symptoms of PE in children may differ from those in adults. Children often have a delayed presentation due to an increased ability to physiologically compensate as compared to adults, non-specific symptoms, and difficulty in symptom communication. These signs and symptoms include chest pain, dyspnea, hypoxemia, cough, hemoptysis, or more severely, hypotension, tachycardia, and cardiac arrest. There should be a high index of suspicion in children with risk factors for PE, which include use of oral contraceptives, hypercoagulable state, presence of an indwelling central venous catheter, obesity, malignancy, sickle cell anemia, and sepsis. \r\n\r\n\r\nSevere pulmonary embolism causes an acute increase in pulmonary artery pressure based on the degree of obstruction. Acute RV dysfunction or failure can lead to RV dilation, tricuspid regurgitation, left ventricular (LV) dysfunction, and cardiac arrest. The combination of systemic hypotension and increased RV pressure leads to a decrease in myocardial oxygen supply with increased demand that results in a downward spiral of myocardial ischemia followed by further mismatch in myocardial oxygen supply and demand. Useful laboratory values include d-dimer, coagulation studies, and cardiac enzymes. The electrocardiogram will often show signs of right ventricular strain. Echocardiography may demonstrate the pulmonary embolism and indirect signs of acute pulmonary hypertension with tricuspid regurgitation, RV dilation, and RV systolic dysfunction. When risk factors, clinical signs and symptoms, and laboratory values suggest a high probability of PE, computed tomography pulmonary angiography (CTPA) is considered the diagnostic test of choice. \r\n\r\n\r\nIn patients with severe high-risk pulmonary embolism, systemic thrombolysis with thrombolytic agents such as tissue plasminogen activator (tPA) has been shown to improve outcomes. This is reflected in guidelines recommending this treatment, with the greatest benefit being initiation within 24 hours of symptom onset. Surgical embolectomy (SE) or catheter-based embolectomy (with or without catheter directed thrombolytic treatment) may also be considered in severe cases, though evidence on outcomes is less robust. In patients with intermediate risk PE, systemic thrombolysis may be associated with less progression of symptoms but is associated with increased risk for severe intracranial bleeding. Retrospective studies in adults have found equivalent short- and long-term mortality between patients receiving systemic thrombolysis versus surgical embolectomy. These studies have found that the thrombolysis patients experienced more stroke, reintervention, and recurrence, as compared to the SE group, which experienced a higher rate of major bleeding. A small retrospective study in children showed similar mortality rate between thrombolysis and SE but higher rates of non-fatal major hemorrhage in patients undergoing SE. Other practical considerations in choosing management are the timing and availability of a surgical team versus catheterization team, how distal the embolus resides, and if the patient has contraindications to systemic thrombolysis. \r\n\r\n\r\nGiven the severity of the signs and symptoms in this patient consistent with a high-risk massive PE with hemodynamic compromise, thrombolytic intervention with tissue plasminogen activator would be indicated to prevent further decompensation. Unfractionated heparin alone would not be sufficient for a high-risk PE but may appropriate for intermediate risk PE. Warfarin alone would not be an appropriate treatment in a patient with high-risk PE because it requires administration for 5 to 7 days to achieve a therapeutic level and has a transient procoagulant effect during initial administration requiring coadministration with either unfractionated heparin or low molecular-weight heparin. \r\n\r\n\r\n \r\nREFERENCES \r\n\r\nRoss C, Kumar R, Pelland-Marcotte MC et al. Acute Management of High-Risk and Intermediate-Risk Pulmonary Embolism in Children: A Review. Chest<\/em>. 2022 161(3):791-802. doi: 10.1016\/j.chest.2021.09.019. \r\n\r\n\r\nZaidi AU, Hutchins KK, Rajpurkar M. Pulmonary Embolism in Children. Front Pediatr<\/em>. 2017;5:170. doi: 10.3389\/fped.2017.00170. \r\n\r\n\r\nOrtel TL, Neumann I, Ageno W, et al. American Society of Hematology 2020 guidelines for management of venous thromboembolism: treatment of deep vein thrombosis and pulmonary embolism. Blood Advances<\/em>. 2020;4(19):4693-4738.\r\n\r\n\r\nKonstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (Ers). Eur Heart J<\/em>. 2020;41(4):543-603.\r\n\r\n\r\nNavanandan N, Stein J, Mistry RD. Pulmonary Embolism in Children. Pediatr Emerg Care<\/em>. 2019:35(2): 143-151.\r\n”,”hint”:””,”answers”:{“yw3nb”:{“id”:”yw3nb”,”image”:””,”imageId”:””,”title”:”A. Unfractionated heparin “},”zgmzc”:{“id”:”zgmzc”,”image”:””,”imageId”:””,”title”:”B. Tissue plasminogen activator”,”isCorrect”:”1″},”rs8ml”:{“id”:”rs8ml”,”image”:””,”imageId”:””,”title”:”C. Warfarin\r\n\r\n”}}}}}

{“questions”:{“5jebq”:{“id”:”5jebq”,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Author: Nicholas Houska, DO – University of Colorado, Children\u2019s Hospital Colorado \r\nA 2-day-old boy born at 31 weeks of gestation with a congenital diaphragmatic hernia develops severe hypoxemia despite utilization of high-frequency oscillatory ventilation. The patient is deemed NOT to be a candidate for extracorporeal membrane oxygenation according to institutional policy. Which of the following adverse outcomes is the MOST likely reason why this patient is not a candidate for extracorporeal membrane oxygenation?\r\n\r\n”,”desc”:”EXPLANATION \r\nThe Extracorporeal Life Support Organization (ELSO) Guidelines for Neonatal Respiratory Failure provide evidence-based guidelines on patient selection, modes of support, and technical considerations for extracorporeal membrane oxygenation (ECMO) in neonates. These 2020 guidelines state that postmenstrual age <34 weeks and weight <2 kg are relative contraindications for ECMO, where postmenstrual age is defined as the sum of gestational age and chronologic age. The reason for this is the historically high rate of intracranial hemorrhage (ICH) (36%) and mortality (62%) in neonates <35 weeks gestational age (GA) versus 12% rate of ICH and 49% mortality in those over 35 weeks gestation.\r\n\r\nWith improvements in mortality trends and the rates of ICH in neonates <34 weeks GA, there is increasing utilization of ECMO in this population. Survival in patients <34 weeks GA who are offered ECMO has increased from 21% to between 48-76%. As survival outcomes continue to improve, certain centers are considering younger and smaller patients as candidates for ECMO. In a 2023 article, Burgos et al suggest that ECMO should be considered for patients at 32 to 33 weeks GA when restricted to high-volume neonatal ECMO centers with close reporting to ELSO, targeted oxygen delivery, and continuous technology development. Despite this, prematurity and extremely low birth weight remain high risk factors for morbidity and mortality with ECMO.\r\n\r\nThe correct answer is B. The risk of intracranial bleeding is the major reason to avoid ECMO in the patient described in the stem. While thromboembolism and infection are both causes of morbidity and mortality in premature infants on ECMO, it is the risk of intracranial hemorrhage due to anticoagulation that is the basis for a relative contraindication to ECMO in patients < 34 weeks postmenstrual age. \r\n\r\n \r\nREFERENCES \r\nWild KT, Rintoul N, Kattan J, Gray B. Extracorporeal Life Support Organization (ELSO): Guidelines for Neonatal Respiratory Failure. ASAIO J<\/em>. 2020;66(5):463-470. \r\n\r\nUpp JR Jr, Bush PE, Zwischenberger JB. Complications of neonatal extracorporeal membrane oxygenation. Perfusion<\/em>. 1994;9(4):241-56.\r\n\r\nBurgos CM, Rintoul N, Broman LM. ECMO for premature neonates- Are we there yet? Seminars in Pediatric Surgery<\/em>. 2023;32(4):151335\r\n\r\n”,”hint”:””,”answers”:{“gczo3”:{“id”:”gczo3″,”image”:””,”imageId”:””,”title”:”A. Thromboembolism “},”2ie8t”:{“id”:”2ie8t”,”image”:””,”imageId”:””,”title”:”B. Intracranial hemorrhage “,”isCorrect”:”1″},”l00qy”:{“id”:”l00qy”,”image”:””,”imageId”:””,”title”:”C. Infection\r\n”}}}}}

{“questions”:{“9xj1q”:{“id”:”9xj1q”,”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 newborn boy with a prenatal diagnosis of Tetralogy of Fallot develops respiratory distress shortly after birth, subsequently requiring intubation and extracorporeal membrane oxygenation. A portable computed tomography scan of the chest demonstrates severe main pulmonary artery dilation and bronchial compression. Which of the following types of Tetralogy of Fallot is the MOST likely diagnosis in this neonate?\r\n”,”desc”:”EXPLANATION \r\nTetralogy of Fallot (TOF) with absent pulmonary valve (TOF\/APV) is a rare type of TOF (3%) associated with high fetal and neonatal morbidity and mortality. In this defect, severe pulmonary insufficiency due to the lack of pulmonary valve cusps leads to massive main and proximal pulmonary artery dilation and thus extrinsic airway compression. Volume and pressure overload of the right ventricle (RV) can lead to dysfunction, and tricuspid regurgitation with associated left ventricular dysfunction. Chromosomal anomalies are found in 46% of TOF\/APV patients who undergo genetic testing, with 35% having the 22q11.2 deletion. The clinical presentation of TOF\/APV lies on a spectrum, ranging from fetal hydrops or severe postnatal respiratory distress to mild cardiopulmonary symptoms during infancy. The necessity for postnatal respiratory or cardiovascular support is common, and many patients do not survive to surgical repair. \r\n\r\nGiven the increased utilization and diagnostic capabilities of fetal imaging and the poor prognosis of TOF\/APV, pregnancy termination is common after prenatal diagnosis. A 2021 study found that in patients with intention to treat after birth, 9% died in utero and 27% died postnatally. Right ventricular dysfunction independently predicted overall mortality, while pulmonary artery z-scores did NOT correlate with outcomes. Management of TOF\/APV includes respiratory support based on symptoms. Patients with mild obstructive symptoms may be supported with medical management, oxygen therapy, or non-invasive positive pressure ventilation until surgical repair. These patients are often prone to frequent respiratory infections, which may require hospitalization. Conversely, patients born with more severe respiratory distress may require prone positioning to alleviate compression and\/or intubation and mechanical ventilation. Patients with the most severe respiratory failure or cardiovascular dysfunction may require extracorporeal membrane oxygenation and early surgical repair. Surgical repair includes addressing the ventricular septal defect, the right ventricular outflow tract with a valved or non-valved conduit, and pulmonary arterioplasty. There have also been case reports of combining cardiac repair of TOF\/APV with external bronchial stenting to relieve airway compression. \r\n\r\nTetralogy of Fallot with Pulmonary Stenosis and Tetralogy of Fallot with Pulmonary Atresia are associated with normal, small, or discontinuous main and\/or branch pulmonary arteries. The patient in the stem has a presentation most consistent with TOF\/APV.\r\n\r\n\r\n \r\nREFERENCES \r\nNuri H, Virgone A. Tetralogy of Fallot and absent pulmonary valve syndrome. Multimed Man Cardiothorac Surg<\/em>. 2022 Nov 8;2022. doi: 10.1510\/mmcts.2022.071\r\n\r\nPinsky WW, Nihill MR, Mullins CE, Harrison G, McNamara DG. The absent pulmonary valve syndrome. Considerations of management. Circulation<\/em>. 1978;57(1):159-162. doi: 10.1161\/01.cir.57.1.159. PMID: 618384.\r\n\r\nChelliah A, Moon-Grady AJ, Peyvandi S, et al. Contemporary outcomes in Tetralogy of Fallot with absent pulmonary valve after fetal diagnosis. J Am Heart Assoc<\/em>. 2021;10(12):e019713.\r\n\r\nSakamoto T, Nagase Y, Hasegawa H, Shin’oka T, Tomimatsu H, Kurosawa H. One-stage intracardiac repair in combination with external stenting of the trachea and right bronchus for tetralogy of Fallot with an absent pulmonary valve and tracheobronchomalacia. J Thorac Cardiovasc Surg<\/em>. 2005;130(6):1717-1718.\r\n\r\n”,”hint”:””,”answers”:{“oz08i”:{“id”:”oz08i”,”image”:””,”imageId”:””,”title”:”A. Tetralogy of Fallot with Pulmonary Stenosis”},”ws0tw”:{“id”:”ws0tw”,”image”:””,”imageId”:””,”title”:”B. Tetralogy of Fallot with Absent Pulmonary Valve”,”isCorrect”:”1″},”969aa”:{“id”:”969aa”,”image”:””,”imageId”:””,”title”:”C. Tetralogy of Fallot with Pulmonary Atresia”}}}}}

{“questions”:{“6u76f”:{“id”:”6u76f”,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Author: Nicholas Houska, DO – University of Colorado, Children\u2019s Hospital Colorado \r\nA five-month-old boy has just undergone repair of a perimembranous ventricular septal defect utilizing cardiopulmonary bypass. Shortly after aortic cross clamp removal, the ECG exhibits ST segment elevation in leads II, III, and AVF. Administration of which of the following drugs is the MOST appropriate treatment?”,”desc”:”EXPLANATION \r\nCongenital cardiac surgery often poses the risk for air to enter the left sided cardiac structures, which can subsequently be embolized to the systemic circulation. Due to its anterior location, the right coronary artery is a common anatomical site for air to travel after release of the aortic cross clamp. This typically presents as ST segment elevation on the ECG and a variable degree of right ventricular dysfunction or arrythmias. Given the spectrum of congenital cardiac lesions, air embolism to the left coronary artery should also be considered in situations where it is anatomically located in a non-dependent area, and if clinical signs are suggestive. Management of coronary air embolism involves increasing the coronary perfusion pressure by increasing the aortic diastolic blood pressure. This often requires co-management between the anesthesiologist, surgeon, and perfusionist to decide the best method to increase diastolic blood pressure. Often a combination of increasing cardiopulmonary bypass flow and administration of vasoactive medications is usually successful. Myocardial dysfunction and ECG changes are typically transient, though this may be a cause of difficulty in separating from cardiopulmonary bypass due to arrythmia or ventricular dysfunction. \r\n\r\nThe correct answer in the scenario is A, administration of phenylephrine to increase the coronary perfusion pressure. Other treatments include increasing the cardiopulmonary bypass pump flow or administration of other vasoactive agents, such as norepinephrine, epinephrine or vasopressin. These treatment options typically provide sufficient pressure to force the air bubbles through the coronary circulation. Administration of nitroglycerin is unlikely to be of benefit as the problem is related to a mechanical obstruction with air rather than coronary vasospasm. Esmolol is not the best option in this clinical scenario, though prevention of tachycardia is helpful to decrease myocardial oxygen demand. \r\n\r\n \r\nREFERENCES \r\nMonaco F, Di Prima AL, Kim JH et al. Management of Challenging Cardiopulmonary Bypass Separation. J Cardiothorac Vasc Anesth<\/em>. 2020;34(6):1622-1635. doi: 10.1053\/j.jvca.2020.02.038. \r\n\r\nSarkar M, Prabhu V. Basics of cardiopulmonary bypass. Indian J Anaesth<\/em>. 2017;61(9):760-767. doi: 10.4103\/ija.IJA_379_17.\r\n”,”hint”:””,”answers”:{“4s6r1”:{“id”:”4s6r1″,”image”:””,”imageId”:””,”title”:”A. Phenylephrine “,”isCorrect”:”1″},”lfmru”:{“id”:”lfmru”,”image”:””,”imageId”:””,”title”:”B. Esmolol”},”kx80v”:{“id”:”kx80v”,”image”:””,”imageId”:””,”title”:”C. Nitroglycerin \r\n\r\n”}}}}}