The Hemodynamic and Holter-Electrocardiogram Changes During Halothane and Sevoflurane Anesthesia for Adenoidectomy in Children Aged One to Three Years

Abstract

Halothane and sevoflurane are volatile anesthetics that are preferred for the inhaled induction of anesthesia in children. High inspired concentrations of 8% sevoflurane results in induction times more rapid than or similar to those with 5% halothane (1,2). The hemodynamic responses to a rapid high induction technique, especially with 5% halothane, have not been studied in small children. There are also few reports comparing sevoflurane and halothane anesthesia with regard to cardiac arrhythmias (3) and none in this age group using Holter-electrocardiogram (ECG) monitoring. Therefore, we designed this study to examine the hemodynamic responses to induction with halothane or sevoflurane and to record the incidence of cardiac arrhythmias during halothane or sevoflurane anesthesia in children aged 1–3 yr. Methods After institutional ethics committee approval and informed written parental consent, 70 children aged 1–3 yr (ASA physical status I and II) undergoing adenoidectomy with or without myringotomy were randomly allocated to received either sevoflurane 8% or halothane 5% for induction of anesthesia. No sedative or anticholinergic premedication was used. At least 15 min before the induction of anesthesia, Holter-ECG recording was started. Preinduction heart rate, noninvasive arterial pressure, and hemoglobin oxygen saturation (SpO2) were recorded. Inhaled anesthesia with either 8% sevoflurane or 5% halothane was used via a facemask with N2O 66% in O2. Tracheal intubation was accomplished without neuromuscular block and was followed by 12.5 mg of diclofenac PR. No opioids were used intraoperatively. Patients received an IV NaCl infusion. Ventilation was controlled to maintain normocapnia. During maintenance of anesthesia, the inspired concentration of the anesthetic (in N2O 66% in O2) was adjusted to maintain arterial pressure within 20% of baseline values. After surgery, the anesthetics were discontinued, and extubation was performed when spontaneous breathing was adequate. Heart rate, SpO2, arterial pressure, and end-tidal anesthetic concentrations were recorded at predetermined time points. Age-adjusted minimum alveolar anesthetic concentration (MAC) values (5,6) (N2O excluded) were calculated for each end-tidal recording during anesthesia, and the MAC-hours were obtained. A physician (HK) blinded to the anesthetic method analyzed the Holter-ECG recordings over four time periods: induction (start of induction to tracheal intubation), intubation (intubation to start of surgery), surgery (start of surgery to extubation), and recovery (extubation until waking in the postanesthesia care unit). Supraventricular extrasystoles (SVEs) or ventricular premature beats (VPBs) were regarded as cardiac arrhythmia if three or more complexes occurred per patient during any of the predetermined time periods. Ventricular (VT) or supraventricular tachycardia (SVT) was defined as three or more consecutive beats at a heart rate of >100 bpm. The incidences of bradycardia (<70 bpm) (4) and tachycardia (>170 bpm) were recorded. Data are presented as mean ± SD or number (percentage). Statistical comparisons were made by using Student’s t-test, the Mann-Whitney U-test, and χ2 or Fisher’s exact test, as appropriate. Changes in heart rate and arterial pressure were analyzed by using two-way analysis of variance for repeated measures with the Spjotvall-Stoline test for post hoc comparisons. A P value <0.05 was considered significant. The sample size was determined on the assumption that the incidence of cardiac arrhythmia during halothane anesthesia would be at least 40% (7), and that during sevoflurane 10% (8). A minimum of 29 patients would be sufficient to detect this difference (α = 0.05, power = 80%). Results All children were aged 1–3 yr. The two groups were comparable in weight, duration of surgery and anesthesia, and MAC-hours (0.41 ± 0.1 in both groups). The MAC value (N2O excluded) at the end of induction was higher with halothane (3.2 MAC) than with sevoflurane (2.1 MAC) (P = 0.0001). Thirty-five patients were recruited in each group. One patient from the sevoflurane group was excluded because of faulty Holter-ECG recording. One patient from the halothane group, who had changes in QRS morphology before and during anesthesia, was also excluded. The overall incidence of cardiac arrhythmias was higher with halothane (23%) than with sevoflurane (6%) (P = 0.04) (Table 1). Most of the arrhythmic episodes were self-limiting SVEs or VPBs, lasting 1–2 min, except in two patients in the halothane group with SVEs lasting 10–15 min. One episode of SVT occurred in one patient with sevoflurane and lasted for three beats. Seven (20%) and 16 (47%) patients in the halothane and sevoflurane groups, respectively, were tachycardic (>170 bpm) during the induction of anesthesia (P = 0.01). Table 1: Electrocardiogram Changes During AnesthesiaThe distributions of the cardiac arrhythmias during anesthesia are shown in Table 2. One patient in the halothane group had SVEs both after intubation and during surgery. Another patient in the halothane group with SVEs during recovery already had SVEs (one to five complexes/min) for 10 min before the induction of anesthesia. Two other patients in the halothane group with SVEs occuring after intubation had concomitant bradycardia (66 and 68 bpm). Two (6%) patients in the halothane group developed laryngospasm after extubation, resulting in SpO2 <90%. One of these halothane patients had a transient episode of SVE, and the other had an episode of VPBs. One halothane patient with desaturation <90% 5 min after arrival in the recovery room had VPBs lasting for nine beats. Table 2: Distribution of Cardiac Arrhythmias During AnesthesiaAfter the induction of anesthesia, heart rate decreased with halothane and increased with sevoflurane. After intubation, heart rate decreased in both groups. Post hoc analysis showed that heart rate was higher with sevoflurane at the end of induction (P = 0.04) and after intubation (P = 0.00003). Mean arterial pressure decreased similarly in both groups in response to the induction of anesthesia and decreased further after intubation. Discussion We examined the incidence of cardiac arrhythmias in children one to three years of age during halothane or sevoflurane anesthesia using a Holter-ECG device. Similar to previous studies (3,8), cardiac arrhythmias during anesthesia were more frequent with halothane (23%) than with sevoflurane (6%). The incidence of bradycardia was similar with the two anesthetics, but tachycardia was more common with sevoflurane, especially during the induction of anesthesia. Apart from one episode of SVT, the arrhythmic episodes in both groups were minor self-limiting SVEs or unifocal VPBs. No episodes of VT or bigeminy were detected in either group. This contrasts sharply with previous studies, in which significant ventricular arrhythmias (multifocal ventricular extrasystoles, VT) have been observed in 20%–45% of children receiving halothane for maintenance of anesthesia for adenoidectomy during spontaneous ventilation (7,9). A possible mechanisms for increased ventricular arrhythmia during spontaneous ventilation could be hypercarbia and increased arterial pressure heart rate and sympathoadrenal catecholamine release (10). More children had cardiac arrhythmias in the recovery period with halothane (P = 0.04). Apart from the one patient with SVEs before anesthesia, all the arrhythmic episodes during the recovery period occurred within 10 minutes after extubation and were associated with desaturation. Children may have been in a deeper level of anesthesia and possibly hypoventilated at the time of awakening. Sevoflurane, with its faster elimination, may provide a greater safety margin in regard to airway patency in the early postoperative period. The overall low incidence of cardiac arrhythmias in our study may have been influenced by the young age of the children, as persistent ventricular arrhythmias have been rarely shown to occur in children less than two years old (11). Depth of anesthesia may also be an important cause of arrhythmia during surgery (11). We controlled the end-tidal concentration of the anesthetics according to the arterial pressure response to surgical stimulus and believe that this provided adequate depth of anesthesia. We used a rapid inhaled induction technique with 5% halothane or 8% sevoflurane. Similar to previous studies (1,2), this technique was well tolerated by the patients. Induction of anesthesia with sevoflurane was associated with an increase in heart rate whereas heart rate decreased with halothane. This may reflect the greater negative inotropic effect of halothane (12) and the higher MAC value at the end of induction. In conclusion, cardiac arrhythmias during inhaled anesthesia with halothane were more frequent than with sevoflurane. The overall incidence of arrhythmias was low in both groups, which was probably related to the use of controlled ventilation and to a sufficient depth of anesthesia. Induction with a high concentration of sevoflurane caused more tachycardia than halothane, but the incidence of bradycardia was similar with both anesthetics. We thank Anneli Innanmaa, RN; Ritva Turtiainen, RN; and the personnel of the ENT surgery unit of Tampere University Hospital for their help and cooperation during this study.