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Is Sevoflurane and Remifentanil Induction of Anesthesia Safe in Children With Severe Dilated Cardiomyopathy?
Is Sevoflurane and Remifentanil Induction of Anesthesia Safe in Children With Severe Dilated Cardiomyopathy? Ibrahim Abu-Shahwan, MD
D
ILATED (CONGESTIVE) CARDIOMYOPATHY is the end result of multiple different disease processes that lead to heart failure.1 Idiopathic dilated cardiomyopathy accounts for 50% of cases. From a functional point of view, dilated cardiomyopathy is associated with dilated cardiac chambers and decreased ventricular systolic function.2 In young children, the symptoms are usually vague and include tachypnea, dyspnea, irritability, and poor feeding. Shortness of breath and exercise intolerance are the most common symptoms in older children. The onset of symptoms is usually gradual and correlates with the degree of myocardial dysfunction. The clinical picture of a patient with dilated cardiomyopathy consists of low cardiac output, fluid retention, and increased vasoconstriction because of neurohumoral activation to maintain adequate perfusion pressure.1 Because of improvements in medical management, more patients with severe cardiomyopathy are coming to the operating room for minor procedures such as central catheter placement, gastrostomy tube insertion, and dental work.3 The anesthetic management of a child with severe dilated cardiomyopathy can be extremely challenging. Cardiovascular collapse is an ever-present threat while administering anesthesia to such patients. High-dose opioid general anesthesia, recommended for patients with hemodynamic instability, is problematic because of the risk of postoperative respiratory depression. Local or regional anesthesia can be inappropriate because of the age of the patient or the surgery itself. A case of severe cardiovascular collapse in a child with dilated cardiomyopathy after the induction of anesthesia with sevoflurane and remifentanil is described. CASE REPORT
DISCUSSION
A 22-month-old child weighing 10.6 kg was admitted to the daycare service for elective dental restoration after having been seen in the preoperative clinic. Her medical history was significant for idiopathic dilated cardiomyopathy, diagnosed at the age of 18 months; congestive heart failure; and ventricular tachycardia. Medications included carvedilol, 4.5 mg twice a day, digoxin, 60 g once a day, furosemide, 5 mg twice a day, captopril, 10 mg 3 times a day, and amiodarone, 50 mg once a day. A preoperative cardiac echocardiogram revealed severe global systolic dysfunction of the left ventricle, moderate dilation of the left ventricle, mild dilation of the right ventricle, moderate regurgitation of the mitral valve, and mild regurgitation of the tricuspid and pulmonary valves. Her ejection fraction was reported to be less than 20%. The child was given oral midazolam, 5 mg, and acetaminophen, 300
From the Department of Anesthesiology, Children Hospital of Eastern Ontario, University of Ottawa, Ottawa, Ontario, Canada. Address reprint requests to Ibrahim Abu-Shahwan, MD, Children’s Hospital of Eastern Ontario, Department of Anesthesiology, University of Ottawa, 401 Smyth Road, Ottawa, ON, K1H 8L1, Canada. E-mail: [email protected] © 2008 Elsevier Inc. All rights reserved. 1053-0770/08/2205-0018$34.00/0 doi:10.1053/j.jvca.2007.06.002 Key words: cardiomyopathy, remifentanil, sevoflurane, anesthesia, pediatric 744
mg, approximately 30 minutes before surgery. Standard monitors including pulse oximetry, electrocardiography, and a blood pressure cuff were applied before anesthesia induction. Oxygen by mask was given during placement of the monitors. Blood pressure (BP) of 80/40 mmHg, heart rate (HR) of 120 beats/min, and 100% oxygen saturation were recorded. The induction of anesthesia started with 3% sevoflurane in oxygen and air. Once an intravenous catheter was in place, a bolus of remifentanil, 1 g/kg, was administered. After remifentanil and before mivacurium administration, there were decreases in HR to 85 bpm and BP to 60/30 mmHg. Mivacurium, 2 mg, was administered after remifentanil to facilitate endotracheal intubation. There was no change in BP or HR after the mivacurium and before intubation. Immediately after laryngoscopy and successful nasal intubation of the trachea, HR decreased to about 25 beats/min followed by the loss of BP, pulse signal, and end-tidal carbon dioxide. Electromechanical dissociation was diagnosed, and cardiopulmonary resuscitation was started with external cardiac compressions and repeated boluses of epinephrine (total dose of 0.4 mg) and atropine (total dose of 0.8 mg). An infusion of dopamine (5 g/kg/min) was also started. After 20 minutes of continuous cardiopulmonary resuscitation, the patient regained her preoperative HR and BP and was transferred to the intensive care unit for monitoring. In the intensive care unit, the patient was kept intubated, ventilated, and monitored with invasive arterial blood pressure and central venous pressure catheters. Dopamine infusion ranged from 5 to 7.5 g/kg/min over this period. Two days after this episode, the patient returned to the operating room with the dopamine infusion at 10 g/kg/min. Anesthesia was induced with repeated small doses of midazolam and fentanyl. Ketamine, 1 mg/kg, was also used. No muscle relaxant was administered, and no inhaled agent was used. Anesthesia was maintained with an infusion of midazolam and fentanyl. No significant hemodynamic changes were noticed during the induction or maintenance of anesthesia.
Anesthesia for patients with dilated cardiomyopathy presents a considerable challenge to the clinician. Dilated cardiomyopathy is associated with abnormally depressed contractile function manifested as decreased ejection fraction and cardiac output. The decline in forward blood flow results in the pooling of intracavitary blood and secondary increases in end-diastolic volume, end-diastolic pressure, and ventricular filling pressure. To maintain an adequate cardiac output, the ventricles dilate and the myocardium hypertrophies to some degree. Ventricular dilatation results in increased wall tension, increased oxygen consumption, and decreased myocardial efficiency. The limitation of ventricular function is associated with increased sympathetic nervous system and renin-angiotensin activity. The activation of these systems contributes to peripheral vascular changes and the clinical picture of congestive heart failure. In patients with dilated cardiomyopathy, adequate HR and preload are needed to maintain cardiac output. Drugs that are vagotonic, such as opioids, may induce bradycardia and decrease cardiac output considerably. The most likely mechanisms contributing to the cardiac arrest in the present case are the vagally-induced severe bradycardia by remifentanil and the centrally mediated decrease in the sympathetic tone secondary to sevoflurane induction. This child required an elevated sympathetic tone and tachycardia to maintain adequate perfusion
Journal of Cardiothoracic and Vascular Anesthesia, Vol 22, No 5 (October), 2008: pp 744-745
SEVOFLURANE AND REMIFENTANIL INDUCTION
745
pressure. This increased tone was presumably decreased after sevoflurane induction and resulted in her inability to mount an adequate sympathetic response to counteract the bradycardia induced centrally by the remifentanil bolus. Laryngoscopy was also an important factor in this patient. It is also known that laryngoscopy can produce an additional increase in vagal tone resulting in severe bradycardia. A contributing role of carvedilol and/or captopril cannot be excluded. Invasive hemodynamic monitoring can be useful because these patients are HR and preload dependent. Sevoflurane is widely used for the induction of general anesthesia in children. Because of its low blood-gas partition coefficient, sevoflurane allows for rapid induction and emergence from anesthesia.4 Sevoflurane is also less arrhythmogenic than halothane.5,6 Inhalation induction of general anesthesia with 8% sevoflurane is rapid and well tolerated by healthy children. However, Townsend and Stokes7 reported the occurrence of profound bradycardia in 4 healthy children aged 6 months to 2 years undergoing minor procedures, with an 8% sevoflurane induction. In all 4 cases, the onset of bradycardia occurred during induction and was not associated with the loss of the airway or ventilation. Sevoflurane 8% also has been reported to cause second-degree atrioventricular block in a 12-year-old healthy female,8 and slow induction of general anesthesia has been associated with complete atrioventricular block in a 10-year-old child with hypertension, renal dysfunction, and impaired cardiac conduction.9
Remifentanil is an ultra–short-acting opioid agonist with a rapid onset and short duration of action. Remifentanil and other potent opioids are frequently used to reduce the hemodynamic response to laryngoscopy and intubation, particularly in patients with heart disease. However, these potent drugs can result in severe bradycardia and even asystole.10-12 It is generally believed that opioid-induced bradycardia is most likely the result of central vagal stimulation.13 The incidence of bradycardia is believed to be higher in anesthetized patients13 and when patients are breathing 100% oxygen.14 The use of adrenergic blockers is also considered to be a predisposing factor for the occurrence of bradycardia in patients receiving remifentanil.15 As far as the author is aware, this is the first reported case of cardiovascular collapse after sevoflurane and remifentanil induction in a pediatric patient. Cardiovascular collapse is an ever-present threat in children with dilated cardiomyopathy while administering anesthetic drugs. These patients require delicate and special care because commonly used anesthetic drugs alone or in combination may have dire consequences. The risk of negative outcome increases with anesthetic agents known to cause myocardial depression and bradycardia. Inadequate anesthesia is another contributing factor, particularly in patients on the verge of sympathetic exhaustion. In these patients, invasive arterial pressure and central venous pressure for monitoring are useful. These patients should not be considered as day-surgery cases.
REFERENCES 1. Allen HD, Gutgesell HP, Clark EB, et al (eds): Moss and Adams’ Heart Disease in Infants, Children, and Adolescents. Philadelphia, PA, Lippincott Williams & Wilkins, 2001, pp 1187-1197 2. Goldberg SJ, Valdes-Cruz LM, Sahn DJ, et al: Two-dimensional echocardiographic evaluation of dilated cardiomyopathy in children. Am J Cardiol 52:1244-1248, 1983 3. Colan S, Spevak P, Parness I, et al: Cardiomyopathy, in Fyler DC (ed): Nadas’ Pediatric Cardiology. Philadelphia, PA, Hanley Belfus, Inc, 1992, pp 329-362 4. Yashuda N, Targ A, Eger E: Solubility of sevoflurane, isoflurane, and halothane in human tissue. Anesth Analg 69:370-373, 1989 5. Lerman J: Pharmacology of inhalational anesthetics in infants and children. Paediatr Anaesth 2:191-203, 1992 6. Kataria B, Epstein R, Bailey A, et al: A comparison of sevoflurane to halothane in pediatric surgical patients: Result of a multicentre international study. Paediatr Anaesth 6:283-292, 1996 7. Townsend P, Stokes MA: Bradycardia during rapid inhalation induction with sevoflurane in children. Br J Anaesth 80:410, 1998 8. Shirley P, Johnston G: Sevoflurane induced atrioventricular block. Paediatr Aanesth 11:125-126, 2001 9. Maruyama K, Agata H, Onon K, et al: Slow induction with sevoflurane was associated with complete atrioventricular block in a
child with hypertension, renal dysfunction, and impaired cardiac conduction. Paediatr Anesth 8:73-78, 1998 10. Egan T, Brock-Utne J: Asystole after anesthesia induction with a fentanyl, propofol, and succinylcholine sequence. Anesth Analg 73:818-820, 1991 11. Schuttler J, Albrecht S, Breivik S, et al: A comparison of remifentanil and alfentanil in patients undergoing major abdominal surgery. Anaesthesia 52:307-317, 1997 12. DeSouza G, Lewis M, TerRiet M: Severe bradycardia after remifentanil. Anesthesiology 87:1019-1020, 1997 13. Reitan J, Stengert K, Wymore M, et al: Central vagal control of fentanyl-induced bradycardia during halothane anesthesia. Anesth Analg 57:31-36, 1978 14. Prakash O, Verdouw P, Dejoung J, et al: Haemodynamic and biochemical variables after induction of anesthesia with fentanyl and nitrous in patients undergoing coronary artery bypass surgery. Can Aanesth Soc J 27:223-229, 1980 15. Dershwitz M, Rnadel G, Rosow C, et al: Initial clinical experience with remifentanil, a new opioid metabolized by esterase. Anesth Analg 81:619-623, 1995
D
ILATED (CONGESTIVE) CARDIOMYOPATHY is the end result of multiple different disease processes that lead to heart failure.1 Idiopathic dilated cardiomyopathy accounts for 50% of cases. From a functional point of view, dilated cardiomyopathy is associated with dilated cardiac chambers and decreased ventricular systolic function.2 In young children, the symptoms are usually vague and include tachypnea, dyspnea, irritability, and poor feeding. Shortness of breath and exercise intolerance are the most common symptoms in older children. The onset of symptoms is usually gradual and correlates with the degree of myocardial dysfunction. The clinical picture of a patient with dilated cardiomyopathy consists of low cardiac output, fluid retention, and increased vasoconstriction because of neurohumoral activation to maintain adequate perfusion pressure.1 Because of improvements in medical management, more patients with severe cardiomyopathy are coming to the operating room for minor procedures such as central catheter placement, gastrostomy tube insertion, and dental work.3 The anesthetic management of a child with severe dilated cardiomyopathy can be extremely challenging. Cardiovascular collapse is an ever-present threat while administering anesthesia to such patients. High-dose opioid general anesthesia, recommended for patients with hemodynamic instability, is problematic because of the risk of postoperative respiratory depression. Local or regional anesthesia can be inappropriate because of the age of the patient or the surgery itself. A case of severe cardiovascular collapse in a child with dilated cardiomyopathy after the induction of anesthesia with sevoflurane and remifentanil is described. CASE REPORT
DISCUSSION
A 22-month-old child weighing 10.6 kg was admitted to the daycare service for elective dental restoration after having been seen in the preoperative clinic. Her medical history was significant for idiopathic dilated cardiomyopathy, diagnosed at the age of 18 months; congestive heart failure; and ventricular tachycardia. Medications included carvedilol, 4.5 mg twice a day, digoxin, 60 g once a day, furosemide, 5 mg twice a day, captopril, 10 mg 3 times a day, and amiodarone, 50 mg once a day. A preoperative cardiac echocardiogram revealed severe global systolic dysfunction of the left ventricle, moderate dilation of the left ventricle, mild dilation of the right ventricle, moderate regurgitation of the mitral valve, and mild regurgitation of the tricuspid and pulmonary valves. Her ejection fraction was reported to be less than 20%. The child was given oral midazolam, 5 mg, and acetaminophen, 300
From the Department of Anesthesiology, Children Hospital of Eastern Ontario, University of Ottawa, Ottawa, Ontario, Canada. Address reprint requests to Ibrahim Abu-Shahwan, MD, Children’s Hospital of Eastern Ontario, Department of Anesthesiology, University of Ottawa, 401 Smyth Road, Ottawa, ON, K1H 8L1, Canada. E-mail: [email protected] © 2008 Elsevier Inc. All rights reserved. 1053-0770/08/2205-0018$34.00/0 doi:10.1053/j.jvca.2007.06.002 Key words: cardiomyopathy, remifentanil, sevoflurane, anesthesia, pediatric 744
mg, approximately 30 minutes before surgery. Standard monitors including pulse oximetry, electrocardiography, and a blood pressure cuff were applied before anesthesia induction. Oxygen by mask was given during placement of the monitors. Blood pressure (BP) of 80/40 mmHg, heart rate (HR) of 120 beats/min, and 100% oxygen saturation were recorded. The induction of anesthesia started with 3% sevoflurane in oxygen and air. Once an intravenous catheter was in place, a bolus of remifentanil, 1 g/kg, was administered. After remifentanil and before mivacurium administration, there were decreases in HR to 85 bpm and BP to 60/30 mmHg. Mivacurium, 2 mg, was administered after remifentanil to facilitate endotracheal intubation. There was no change in BP or HR after the mivacurium and before intubation. Immediately after laryngoscopy and successful nasal intubation of the trachea, HR decreased to about 25 beats/min followed by the loss of BP, pulse signal, and end-tidal carbon dioxide. Electromechanical dissociation was diagnosed, and cardiopulmonary resuscitation was started with external cardiac compressions and repeated boluses of epinephrine (total dose of 0.4 mg) and atropine (total dose of 0.8 mg). An infusion of dopamine (5 g/kg/min) was also started. After 20 minutes of continuous cardiopulmonary resuscitation, the patient regained her preoperative HR and BP and was transferred to the intensive care unit for monitoring. In the intensive care unit, the patient was kept intubated, ventilated, and monitored with invasive arterial blood pressure and central venous pressure catheters. Dopamine infusion ranged from 5 to 7.5 g/kg/min over this period. Two days after this episode, the patient returned to the operating room with the dopamine infusion at 10 g/kg/min. Anesthesia was induced with repeated small doses of midazolam and fentanyl. Ketamine, 1 mg/kg, was also used. No muscle relaxant was administered, and no inhaled agent was used. Anesthesia was maintained with an infusion of midazolam and fentanyl. No significant hemodynamic changes were noticed during the induction or maintenance of anesthesia.
Anesthesia for patients with dilated cardiomyopathy presents a considerable challenge to the clinician. Dilated cardiomyopathy is associated with abnormally depressed contractile function manifested as decreased ejection fraction and cardiac output. The decline in forward blood flow results in the pooling of intracavitary blood and secondary increases in end-diastolic volume, end-diastolic pressure, and ventricular filling pressure. To maintain an adequate cardiac output, the ventricles dilate and the myocardium hypertrophies to some degree. Ventricular dilatation results in increased wall tension, increased oxygen consumption, and decreased myocardial efficiency. The limitation of ventricular function is associated with increased sympathetic nervous system and renin-angiotensin activity. The activation of these systems contributes to peripheral vascular changes and the clinical picture of congestive heart failure. In patients with dilated cardiomyopathy, adequate HR and preload are needed to maintain cardiac output. Drugs that are vagotonic, such as opioids, may induce bradycardia and decrease cardiac output considerably. The most likely mechanisms contributing to the cardiac arrest in the present case are the vagally-induced severe bradycardia by remifentanil and the centrally mediated decrease in the sympathetic tone secondary to sevoflurane induction. This child required an elevated sympathetic tone and tachycardia to maintain adequate perfusion
Journal of Cardiothoracic and Vascular Anesthesia, Vol 22, No 5 (October), 2008: pp 744-745
SEVOFLURANE AND REMIFENTANIL INDUCTION
745
pressure. This increased tone was presumably decreased after sevoflurane induction and resulted in her inability to mount an adequate sympathetic response to counteract the bradycardia induced centrally by the remifentanil bolus. Laryngoscopy was also an important factor in this patient. It is also known that laryngoscopy can produce an additional increase in vagal tone resulting in severe bradycardia. A contributing role of carvedilol and/or captopril cannot be excluded. Invasive hemodynamic monitoring can be useful because these patients are HR and preload dependent. Sevoflurane is widely used for the induction of general anesthesia in children. Because of its low blood-gas partition coefficient, sevoflurane allows for rapid induction and emergence from anesthesia.4 Sevoflurane is also less arrhythmogenic than halothane.5,6 Inhalation induction of general anesthesia with 8% sevoflurane is rapid and well tolerated by healthy children. However, Townsend and Stokes7 reported the occurrence of profound bradycardia in 4 healthy children aged 6 months to 2 years undergoing minor procedures, with an 8% sevoflurane induction. In all 4 cases, the onset of bradycardia occurred during induction and was not associated with the loss of the airway or ventilation. Sevoflurane 8% also has been reported to cause second-degree atrioventricular block in a 12-year-old healthy female,8 and slow induction of general anesthesia has been associated with complete atrioventricular block in a 10-year-old child with hypertension, renal dysfunction, and impaired cardiac conduction.9
Remifentanil is an ultra–short-acting opioid agonist with a rapid onset and short duration of action. Remifentanil and other potent opioids are frequently used to reduce the hemodynamic response to laryngoscopy and intubation, particularly in patients with heart disease. However, these potent drugs can result in severe bradycardia and even asystole.10-12 It is generally believed that opioid-induced bradycardia is most likely the result of central vagal stimulation.13 The incidence of bradycardia is believed to be higher in anesthetized patients13 and when patients are breathing 100% oxygen.14 The use of adrenergic blockers is also considered to be a predisposing factor for the occurrence of bradycardia in patients receiving remifentanil.15 As far as the author is aware, this is the first reported case of cardiovascular collapse after sevoflurane and remifentanil induction in a pediatric patient. Cardiovascular collapse is an ever-present threat in children with dilated cardiomyopathy while administering anesthetic drugs. These patients require delicate and special care because commonly used anesthetic drugs alone or in combination may have dire consequences. The risk of negative outcome increases with anesthetic agents known to cause myocardial depression and bradycardia. Inadequate anesthesia is another contributing factor, particularly in patients on the verge of sympathetic exhaustion. In these patients, invasive arterial pressure and central venous pressure for monitoring are useful. These patients should not be considered as day-surgery cases.
REFERENCES 1. Allen HD, Gutgesell HP, Clark EB, et al (eds): Moss and Adams’ Heart Disease in Infants, Children, and Adolescents. Philadelphia, PA, Lippincott Williams & Wilkins, 2001, pp 1187-1197 2. Goldberg SJ, Valdes-Cruz LM, Sahn DJ, et al: Two-dimensional echocardiographic evaluation of dilated cardiomyopathy in children. Am J Cardiol 52:1244-1248, 1983 3. Colan S, Spevak P, Parness I, et al: Cardiomyopathy, in Fyler DC (ed): Nadas’ Pediatric Cardiology. Philadelphia, PA, Hanley Belfus, Inc, 1992, pp 329-362 4. Yashuda N, Targ A, Eger E: Solubility of sevoflurane, isoflurane, and halothane in human tissue. Anesth Analg 69:370-373, 1989 5. Lerman J: Pharmacology of inhalational anesthetics in infants and children. Paediatr Anaesth 2:191-203, 1992 6. Kataria B, Epstein R, Bailey A, et al: A comparison of sevoflurane to halothane in pediatric surgical patients: Result of a multicentre international study. Paediatr Anaesth 6:283-292, 1996 7. Townsend P, Stokes MA: Bradycardia during rapid inhalation induction with sevoflurane in children. Br J Anaesth 80:410, 1998 8. Shirley P, Johnston G: Sevoflurane induced atrioventricular block. Paediatr Aanesth 11:125-126, 2001 9. Maruyama K, Agata H, Onon K, et al: Slow induction with sevoflurane was associated with complete atrioventricular block in a
child with hypertension, renal dysfunction, and impaired cardiac conduction. Paediatr Anesth 8:73-78, 1998 10. Egan T, Brock-Utne J: Asystole after anesthesia induction with a fentanyl, propofol, and succinylcholine sequence. Anesth Analg 73:818-820, 1991 11. Schuttler J, Albrecht S, Breivik S, et al: A comparison of remifentanil and alfentanil in patients undergoing major abdominal surgery. Anaesthesia 52:307-317, 1997 12. DeSouza G, Lewis M, TerRiet M: Severe bradycardia after remifentanil. Anesthesiology 87:1019-1020, 1997 13. Reitan J, Stengert K, Wymore M, et al: Central vagal control of fentanyl-induced bradycardia during halothane anesthesia. Anesth Analg 57:31-36, 1978 14. Prakash O, Verdouw P, Dejoung J, et al: Haemodynamic and biochemical variables after induction of anesthesia with fentanyl and nitrous in patients undergoing coronary artery bypass surgery. Can Aanesth Soc J 27:223-229, 1980 15. Dershwitz M, Rnadel G, Rosow C, et al: Initial clinical experience with remifentanil, a new opioid metabolized by esterase. Anesth Analg 81:619-623, 1995