Journal of Clinical Anesthesia (2014) 26, 255–256
Editorial
Cardiac dysrhythmias in pediatric patients during general anesthesia Supraventricular dysrhythmias have been observed in about 60% to 80% of surgical patients receiving anesthesia [1,2]. This occurrence has led researchers to focus on the effect of anesthesia on atrial and atrioventricular (AV) nodal electrophysiologic properties associated with the pathogenesis of supraventricular tachycardia (SVT) [3]. Most intraoperative cardiac dysrhythmias may be shortlived and/or have minimal hemodynamic effects, but sustained tachyarrhythmia may cause impairment of cardiovascular function. Halothane was the leading anesthetic causing cardiac dysrhythmias; however, the discontinuation of its use has not stopped the occurrence of intraoperative cardiac dysrhythmias [4]. Cardiac dysrhythmias still occur, although infrequently, in otherwise healthy children receiving general anesthesia [5]. Cardiac dysrhythmias can be a normal physiologic response of the heart to stress, anxiety, pain, infection, and/or medications. True or pathological dysrhythmias, caused by reentry or other congenital and/or acquired pathology, may also occur in pediatric patients. Supraventricular tachycardia is the most common cardiac dysrhythmia observed in otherwise healthy children [6]. The definition of SVT varies according to a child’s age because normal heart rate (HR) in children is age-dependent. Although SVT is not well defined in children, the prevalence of SVT is estimated to be between one in 250 (0.4%) and one in 25,000 (0.04%) [7,8]. Supraventricular tachycardias are usually paroxysmal and characterized by abrupt onset and termination. The diagnosis of true or pathological SVT is based on clinical suspicion that includes a history of paroxysmal episodes of palpitations and a physical examination demonstrating tachycardia. Twenty-four-hour Holter monitoring or an electrophysiologic study is usually required to confirm the diagnosis. The underlying electrophysiologic mechanisms of true or pathological SVT include alteration in normal or abnormal automaticity, triggered activity, and reentrant excitation or combinations of these [2,9]. Based on the type of tachyarrhythmia, its duration and associated hemodynamic changes, as well as how easily it http://dx.doi.org/10.1016/j.jclinane.2014.04.007 0952-8180/© 2014 Elsevier Inc. All rights reserved.
can be terminated with a simple maneuver (vagal maneuver) or pharmacologic intervention (adenosine), the occurrence of perioperative SVT may lead to cancellation of planned surgery, postoperative disposition to escalated care, and/or the need for additional work-up. Perioperative SVTs may be caused by altered characteristics of these otherwise healthy patients; thus, one must determine the causes of the tachycardic episodes and investigate their short-term and long-term outcomes as well as document the treatment administered [9,10]. However, most sustained SVTs are thought to be caused by reentrant excitation [2,9]. Data from the existing literature indicate that anesthetics may directly or indirectly modulate cardiac automaticity and trigger activity via interaction with circulating catecholamines. However, the effects of anesthesia on the substrates of reentrant SVT remain unclear. Anesthetics [intravenous (IV) and inhalational] are known to modulate atrial conduction velocity, repolarization, and refractoriness in their distinctively different ways. For example, IV anesthetics such as thiopental sodium, propofol, and ketamine cause significantly different effects on frequency-dependent AV nodal conduction delay, while inhalational anesthetics such as halothane, isoflurane, or desflurane cause markedly different concentration-dependent effects on atrial conduction, repolarization, and refractoriness and on AV nodal function. Thus, depending on the electrophysiologic effects of the individual anesthetic on the atrium and AV node, a patient may experience different intraoperative cardiac dysrhythmias. Although SVT is the most common cardiac dysrhythmia in otherwise healthy children, the prevalence of SVT during anesthesia was not always fully appreciated. Cripe and his colleagues at Children’s Hospital of Philadelphia present a case series in this issue in the Journal of Clinical Anesthesia in an attempt to determine the characteristics of patients with intraoperative tachycardias, determine the causes of the tachycardic episodes, and investigate the short-term and long-term outcomes as well as the treatment administered. The researchers conducted retrospective anesthesia record reviews over a period of 13 years (from June 1998 to June
256 2011) using HR N 180 beats per minute (bpm) as a definition of SVT, various keywords, and specific medications administered. Using their criteria, the authors identified 36 subjects out of a total 285,353 cases (0.012615%), which is much lower than the prevalence noted in otherwise healthy children without general anesthesia. Does this retrospective data report suggest that anesthetics actually had the opposite effect from that seen in experimental animal studies, in that they suppressed the cardiac automaticity and activity and prevented the reentrant type of SVT? Or is this merely a result of underestimation owing to exclusion criteria? The researchers were not able to connect intraoperative SVT to patient characteristics, to specific surgery, or to anesthetic agents used. Although the majority of children received escalated care after intraoperative SVTs, only three patients (3/36) were discharged with oral antiarrhythmic agents and none had a cardiac anomaly. As Cripe and colleagues mention, it is not easy to distinguish whether patients’ tachycardias represent a true or pathological reentrant SVT or a sinus tachycardia using surface electrocardiogram (ECG) alone. With the advancement of monitoring and electronic medical records, it should be possible to conduct a prospective study to document SVT or any cardiac dysrhythmia during a pediatric anesthesia case series by either embedding an algorithm in the ECG monitor to differentiate SVT from sinus tachycardia or to capture various types of tachycardias and record them simultaneously with the anesthesia record so that the recorded data can be later analyzed to confirm the diagnosis and the conditions associated with the cardiac dysrhythmia. At the present time, we still have to react to a rapidly determined working diagnosis when facing tachyarrhythmia during surgery so that appropriate interventions may be administered in a timely manner so as to prevent impairment of cardiovascular function. In the near future, we should be able to take advantage of emerging technology to enhance our ability to determine the specific type of tachycardia and deliver appropriate treatment. Furthermore, we will be able to assess the prevalence of various cardiac dysrhythmias and the specific effect of anesthesia on cardiac automaticity and excitability, as well as to improve understanding of underlying pathophysiology and etiologies.
Editorial Debra E. Morrison, MD (Health Sciences Clinical Professor) Department of Anesthesiology and Perioperative Care University of California, Irvine Orange, CA 92868, USA E-mail address: [email protected] Shu-Ming Wang, MD (Professor in Residence, Clinical Professor) Department of Anesthesiology and Perioperative Care University of California, Irvine Orange, CA 92868, USA Department of Anesthesia University of Connecticut Farmington, CT 06030, USA E-mail addresses: [email protected] [email protected]
References [1] Raatikainen MJ, Napolitano CA, Druzgala P, Dennis DM. Electrophysiological effects of a novel, short-acting and potent ester derivative of amiodarone, ATI-2001, in guinea pig isolated heart. J Pharmacol Exp Ther 1996;277:1454-63. [2] Atlee JL. Perioperative cardiac dysrhythmias: diagnosis and management. Anesthesiology 1997;86:1397-424. [3] Rodrigo MR, Moles TM, Lee PK. Comparison of the incidence and nature of cardiac arrhythmias occurring during isoflurane or halothane anaesthesia. Studies during dental surgery. Br J Anaesth 1986;58: 394-400. [4] Oh AY, Yun MJ, Kim HJ, Kim HS. Comparison of desflurane with sevoflurane for the incidence of oculocardiac reflex in children undergoing strabismus surgery. Br J Anaesth 2007;99:262-5. [5] Cripe CC, Patel AR, Markowitz SD, Behringer TS, Litman RS. Supraventricular tachycardia during pediatric anesthesia: a case series and qualitative analysis. J Clin Anesth 2014;26:257-63. [6] Josephson ME, Wellens HJ. Differential diagnosis of supraventricular tachycardia. Cardiol Clin 1990;8:411-42. [7] Keith JD, Rowe RD, Vlad P. Heart disease in infancy and childhood. New York: Macmillan; 1967. p. 1056. [8] Ludomirsky A, Garson A Jr. Supraventricular tachycardia. In: Gillette PC, Garson A Jr, editors. Pediatric Arrhythmias: Electrophysiology and Pacing. Philadelphia: WB Saunders; 1990. p. 380. [9] Obel OA, Camm AJ. Supraventricular tachycardia. ECG diagnosis and anatomy. Eur Heart J 1997;18(Suppl C): C2-11. [10] Atlee JL, Dennis DM. Cardiac dysrhythmias. In: Gravenstein N, Kirby RR, editors. Complications in Anesthesiology. Philadelphia: Lippincott-Raven; 1996. p. 281-319.
Editorial
Cardiac dysrhythmias in pediatric patients during general anesthesia Supraventricular dysrhythmias have been observed in about 60% to 80% of surgical patients receiving anesthesia [1,2]. This occurrence has led researchers to focus on the effect of anesthesia on atrial and atrioventricular (AV) nodal electrophysiologic properties associated with the pathogenesis of supraventricular tachycardia (SVT) [3]. Most intraoperative cardiac dysrhythmias may be shortlived and/or have minimal hemodynamic effects, but sustained tachyarrhythmia may cause impairment of cardiovascular function. Halothane was the leading anesthetic causing cardiac dysrhythmias; however, the discontinuation of its use has not stopped the occurrence of intraoperative cardiac dysrhythmias [4]. Cardiac dysrhythmias still occur, although infrequently, in otherwise healthy children receiving general anesthesia [5]. Cardiac dysrhythmias can be a normal physiologic response of the heart to stress, anxiety, pain, infection, and/or medications. True or pathological dysrhythmias, caused by reentry or other congenital and/or acquired pathology, may also occur in pediatric patients. Supraventricular tachycardia is the most common cardiac dysrhythmia observed in otherwise healthy children [6]. The definition of SVT varies according to a child’s age because normal heart rate (HR) in children is age-dependent. Although SVT is not well defined in children, the prevalence of SVT is estimated to be between one in 250 (0.4%) and one in 25,000 (0.04%) [7,8]. Supraventricular tachycardias are usually paroxysmal and characterized by abrupt onset and termination. The diagnosis of true or pathological SVT is based on clinical suspicion that includes a history of paroxysmal episodes of palpitations and a physical examination demonstrating tachycardia. Twenty-four-hour Holter monitoring or an electrophysiologic study is usually required to confirm the diagnosis. The underlying electrophysiologic mechanisms of true or pathological SVT include alteration in normal or abnormal automaticity, triggered activity, and reentrant excitation or combinations of these [2,9]. Based on the type of tachyarrhythmia, its duration and associated hemodynamic changes, as well as how easily it http://dx.doi.org/10.1016/j.jclinane.2014.04.007 0952-8180/© 2014 Elsevier Inc. All rights reserved.
can be terminated with a simple maneuver (vagal maneuver) or pharmacologic intervention (adenosine), the occurrence of perioperative SVT may lead to cancellation of planned surgery, postoperative disposition to escalated care, and/or the need for additional work-up. Perioperative SVTs may be caused by altered characteristics of these otherwise healthy patients; thus, one must determine the causes of the tachycardic episodes and investigate their short-term and long-term outcomes as well as document the treatment administered [9,10]. However, most sustained SVTs are thought to be caused by reentrant excitation [2,9]. Data from the existing literature indicate that anesthetics may directly or indirectly modulate cardiac automaticity and trigger activity via interaction with circulating catecholamines. However, the effects of anesthesia on the substrates of reentrant SVT remain unclear. Anesthetics [intravenous (IV) and inhalational] are known to modulate atrial conduction velocity, repolarization, and refractoriness in their distinctively different ways. For example, IV anesthetics such as thiopental sodium, propofol, and ketamine cause significantly different effects on frequency-dependent AV nodal conduction delay, while inhalational anesthetics such as halothane, isoflurane, or desflurane cause markedly different concentration-dependent effects on atrial conduction, repolarization, and refractoriness and on AV nodal function. Thus, depending on the electrophysiologic effects of the individual anesthetic on the atrium and AV node, a patient may experience different intraoperative cardiac dysrhythmias. Although SVT is the most common cardiac dysrhythmia in otherwise healthy children, the prevalence of SVT during anesthesia was not always fully appreciated. Cripe and his colleagues at Children’s Hospital of Philadelphia present a case series in this issue in the Journal of Clinical Anesthesia in an attempt to determine the characteristics of patients with intraoperative tachycardias, determine the causes of the tachycardic episodes, and investigate the short-term and long-term outcomes as well as the treatment administered. The researchers conducted retrospective anesthesia record reviews over a period of 13 years (from June 1998 to June
256 2011) using HR N 180 beats per minute (bpm) as a definition of SVT, various keywords, and specific medications administered. Using their criteria, the authors identified 36 subjects out of a total 285,353 cases (0.012615%), which is much lower than the prevalence noted in otherwise healthy children without general anesthesia. Does this retrospective data report suggest that anesthetics actually had the opposite effect from that seen in experimental animal studies, in that they suppressed the cardiac automaticity and activity and prevented the reentrant type of SVT? Or is this merely a result of underestimation owing to exclusion criteria? The researchers were not able to connect intraoperative SVT to patient characteristics, to specific surgery, or to anesthetic agents used. Although the majority of children received escalated care after intraoperative SVTs, only three patients (3/36) were discharged with oral antiarrhythmic agents and none had a cardiac anomaly. As Cripe and colleagues mention, it is not easy to distinguish whether patients’ tachycardias represent a true or pathological reentrant SVT or a sinus tachycardia using surface electrocardiogram (ECG) alone. With the advancement of monitoring and electronic medical records, it should be possible to conduct a prospective study to document SVT or any cardiac dysrhythmia during a pediatric anesthesia case series by either embedding an algorithm in the ECG monitor to differentiate SVT from sinus tachycardia or to capture various types of tachycardias and record them simultaneously with the anesthesia record so that the recorded data can be later analyzed to confirm the diagnosis and the conditions associated with the cardiac dysrhythmia. At the present time, we still have to react to a rapidly determined working diagnosis when facing tachyarrhythmia during surgery so that appropriate interventions may be administered in a timely manner so as to prevent impairment of cardiovascular function. In the near future, we should be able to take advantage of emerging technology to enhance our ability to determine the specific type of tachycardia and deliver appropriate treatment. Furthermore, we will be able to assess the prevalence of various cardiac dysrhythmias and the specific effect of anesthesia on cardiac automaticity and excitability, as well as to improve understanding of underlying pathophysiology and etiologies.
Editorial Debra E. Morrison, MD (Health Sciences Clinical Professor) Department of Anesthesiology and Perioperative Care University of California, Irvine Orange, CA 92868, USA E-mail address: [email protected] Shu-Ming Wang, MD (Professor in Residence, Clinical Professor) Department of Anesthesiology and Perioperative Care University of California, Irvine Orange, CA 92868, USA Department of Anesthesia University of Connecticut Farmington, CT 06030, USA E-mail addresses: [email protected] [email protected]
References [1] Raatikainen MJ, Napolitano CA, Druzgala P, Dennis DM. Electrophysiological effects of a novel, short-acting and potent ester derivative of amiodarone, ATI-2001, in guinea pig isolated heart. J Pharmacol Exp Ther 1996;277:1454-63. [2] Atlee JL. Perioperative cardiac dysrhythmias: diagnosis and management. Anesthesiology 1997;86:1397-424. [3] Rodrigo MR, Moles TM, Lee PK. Comparison of the incidence and nature of cardiac arrhythmias occurring during isoflurane or halothane anaesthesia. Studies during dental surgery. Br J Anaesth 1986;58: 394-400. [4] Oh AY, Yun MJ, Kim HJ, Kim HS. Comparison of desflurane with sevoflurane for the incidence of oculocardiac reflex in children undergoing strabismus surgery. Br J Anaesth 2007;99:262-5. [5] Cripe CC, Patel AR, Markowitz SD, Behringer TS, Litman RS. Supraventricular tachycardia during pediatric anesthesia: a case series and qualitative analysis. J Clin Anesth 2014;26:257-63. [6] Josephson ME, Wellens HJ. Differential diagnosis of supraventricular tachycardia. Cardiol Clin 1990;8:411-42. [7] Keith JD, Rowe RD, Vlad P. Heart disease in infancy and childhood. New York: Macmillan; 1967. p. 1056. [8] Ludomirsky A, Garson A Jr. Supraventricular tachycardia. In: Gillette PC, Garson A Jr, editors. Pediatric Arrhythmias: Electrophysiology and Pacing. Philadelphia: WB Saunders; 1990. p. 380. [9] Obel OA, Camm AJ. Supraventricular tachycardia. ECG diagnosis and anatomy. Eur Heart J 1997;18(Suppl C): C2-11. [10] Atlee JL, Dennis DM. Cardiac dysrhythmias. In: Gravenstein N, Kirby RR, editors. Complications in Anesthesiology. Philadelphia: Lippincott-Raven; 1996. p. 281-319.
