Nodal rhythm and bradycardia during inhalation induction with sevoflurane in infants: a comparison of incremental and high-concentration techniques

D. H. Green1, P. Townsend1, O. Bagshaw2 and M. A. Stokes1,2,*

1Department of Anaesthesia and Intensive Care, University of Birmingham, Edgbaston, Birmingham B15 2TH, UK. 2Department of Anaesthesia, Birmingham Children’s Hospital, Steelhouse Lane, Birmingham B4 6NH, UK

Accepted for publication: April 16, 2000


    Abstract
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
We studied heart rate and rhythm changes during sevoflurane inhalation induction in 60 healthy, unpremedicated infants. Patients were allocated randomly to receive an incremental (2% sevoflurane, increased every four to six breaths by 2% increments, to 8%) or high-concentration induction technique (8% sevoflurane from the outset). The ECG was recorded for 330 s (30 s pre- and 300 s postinduction) using a mini-Holter device (Recollect Dual Channel, Hertford Medical) and later analysed by an independent observer. Twelve patients developed nodal rhythm (six in each group), but no other dysrhythmias were recorded. The onset of nodal rhythm was associated with bradycardia (<80 bpm) in seven out of 12 cases, and occurred significantly earlier in the high-concentration group (median 123 (range 99–139) s versus 164 (127–238) s). Its duration was similar in both groups (62 (2–84) s versus 90 (20–167) s). These findings highlight the importance of using continuous ECG analysis when studying volatile anaesthetic agents in young children.

Br J Anaesth 2000; 85: 368–70

Keywords: anaesthesia, paediatric; anaesthetics volatile, sevoflurane; heart


    Introduction
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
Sevoflurane is frequently used for inhalation induction of anaesthesia in children, with little evidence of cardiovascular side effects.1 2 Recent reports, however, suggest that some children may experience significant bradycardia or cardiac conduction abnormalities.3 4 The aim of this study was to investigate heart rate and rhythm changes during inhalation induction of anaesthesia with sevoflurane in infants using either incremental or high-concentration techniques.


    Patients and methods
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
With local research ethics committee approval and parental consent, we recruited 60 healthy, unpremedicated infants, aged 6 weeks to 20 months presenting for elective surgery. We excluded children with known cardiac and respiratory disease, and those on medications known to affect cardiac conduction. Subjects were allocated randomly to receive either incremental or high-concentration sevoflurane using a computer-generated random number allocation and closed-envelope technique. Anaesthesia was induced in the anaesthetic room with the child either cradled on a parent’s lap or supine on an anaesthetic trolley. Electrocardiograph (ECG) monitoring was commenced before induction using a mini-Holter device (Recollect Dual Channel, Hertford Medical). This is a programmable and portable system that uses four electrodes to monitor the bipolar lead CM5 for a period of up to 45 min with dual channel recording. Data are recorded on 1 megabyte of removable RAM which can then be downloaded and analysed further using the accompanying computer software. We programmed the Recollect device to record the ECG for 30 s pre- and 300 s postinduction. All patients were monitored with pulse oximetry. We did not attempt to record systemic arterial pressure during induction because we did not want the stimulus of an inflating cuff to influence measurement of heart rate.

In the incremental group (group I), 2% sevoflurane was introduced via a well-fitting face mask in 33% oxygen in nitrous oxide (total flow 6 litres min–1) through a Jackson-Rees modification of the Ayre’s T-piece. The sevoflurane concentration was increased by 2% every four–six breaths up to a maximum of 8%. In the high-concentration group (group H), the anaesthetic circuit was primed with 8% sevoflurane in 33% oxygen in nitrous oxide before induction. After loss of eyelash reflex, the sevoflurane concentration was decreased to 5% until depth of anaesthesia was judged sufficient to allow i.v. cannulation. At the end of the study period, Holter monitoring was stopped and replaced by conventional three-lead ECG and non-invasive arterial pressure monitoring. Airway complications and arterial haemoglobin oxygen saturation (SpO2) below 95% were noted.

Pre- and postinduction ECG recordings were analysed for changes in heart rate and rhythm by an observer blinded to the method of induction. Bradycardia was defined as a heart rate of <80 bpm. Nodal rhythm was identified when the P wave closely preceded, occurred within, or followed the QRS complex. Data were analysed using Student’s t-test and the Mann–Whitney test, and presented as mean (SD) or median (range) as appropriate. The sample size required to detect a difference of 20 bpm in heart rate between the two groups was calculated at 48 (power of 0.8) and 65 (power of 0.9) based on results from a pilot study. A P-value of <0.05 was taken to be statistically significant.


    Results
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
A total of 60 infants were enrolled in the study: 29 in group I and 31 in group H. The two groups were comparable in age, sex and weight (Table 1), and type of surgical procedure. In each group there were 17 general and three orthopaedic surgical procedures. Plastic and other peripheral surgical procedures accounted for nine cases in group I, and 11 cases in group H. One patient was withdrawn from group I due to technical difficulties resulting in the loss of the ECG recording. This patient was excluded from further analysis.


View this table:
[in this window]
[in a new window]
 
Table 1 Patient characteristics (mean (SD))
 
Pre-induction, and minimum and maximum heart rate during induction did not differ between the groups (Table 2). There were no pre-existing cardiac conduction abnormalities detected, and pre-induction heart rates were in line with previously documented resting heart rates in awake infants.5 The majority of patients remained in sinus rhythm throughout. However, six patients in each group developed a nodal rhythm. An example of the onset of nodal rhythm is shown in Fig. 1. This subgroup of 12 patients was comparable in age to the study population (8.3 (4.2) months versus 7.8 (5.3) months, respectively). There was a significant difference in onset time of nodal rhythm between the groups with onset being earlier in group H 123 (99–139) s versus 164 (127–238) s in group I (Fig. 2). The duration of nodal rhythm was similar in both groups: 62 (2–84) s in group I and 90 (20–167) s in group H (P=0.179). The change in rhythm was associated with bradycardia in seven of the 12 cases (three in group I and four in group H). Of the 47 patients who remained in sinus rhythm throughout induction, only one patient had a decrease in heart rate to less than 80 bpm. There were no other ventricular or supraventricular dysrhythmias recorded during the study period.


View this table:
[in this window]
[in a new window]
 
Table 2 Pre-induction, minimum and maximum heart rate (mean (SD))
 


View larger version (48K):
[in this window]
[in a new window]
 
Fig 1 An example of onset of nodal rhythm during sevoflurane induction in an infant.

 


View larger version (10K):
[in this window]
[in a new window]
 
Fig 2 Onset time of nodal rhythm in incremental group (I) and high-concentration group (H). Box and whisker plots show median, 25th and 75th centiles, and range (*P=0.015).

 
Three patients had an episode of arterial haemoglobin oxygen desaturation (SpO2 <95%) during induction, but none of these was associated with heart rate or rhythm changes.


    Discussion
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
Under the study conditions described, detailed analysis of the ECG recorded during inhalation induction of anaesthesia with sevoflurane in healthy unpremedicated infants demonstrated a 20% incidence of nodal rhythm irrespective of inhalation technique. This finding surprised us because previous studies of inhalation induction of anaesthesia with sevoflurane in young children have not highlighted rhythm disturbance. In a comparison of rapid (8%) sevoflurane induction with 5% halothane in young children (aged 3 months to 3 yr), conduction abnormalities were not a significant problem.6 It is noteworthy, however, that both groups were premedicated with atropine. Under conditions where a deep level of inhalation anaesthesia is required for relatively short duration, such as paediatric bronchoscopy, nodal rhythm may occur with sevoflurane, although the incidence of this and other dysrhythmias is much less than when using halothane.2

In our study, the onset of nodal rhythm was significantly earlier in the high-concentration group, but the duration was similar in both groups. This may be because the development of nodal rhythm is related to depth of anaesthesia. In addition, immaturity of the autonomic nervous system in infants makes this group particularly susceptible to the effects of volatile anaesthetic agents on cardiac conduction pathways. The failure of previous studies to document conduction abnormalities may reflect the method of ECG recording utilized. The poor quality of some single lead (lead II) rhythm strip recordings may not enable accurate analysis. In a comparison of the incidence and nature of arrhythmias using halothane or sevoflurane in paediatric dental anaesthesia,7 Holter monitoring detected a high incidence of arrhythmias (48% versus 16%). Despite simultaneous conventional ECG monitoring, some of these were undetected by the anaesthetist (personal communication). In clinical studies of inhalation agents in children, the precise method of ECG analysis is often not clarified.

A potential criticism of our study is that systemic arterial pressure was not recorded during induction. However, the clinical usefulness of non-invasive arterial pressure measurement during an inhalation induction of anaesthesia in infants is limited, and the validity of intermittent measurements during a dysrhythmia is questionable. Invasive arterial pressure monitoring could not be justified in this study population. Once the induction and ECG recording phases were complete, non-invasive arterial pressure and other monitoring commenced in the usual manner, by which time all infants were in sinus rhythm with age-appropriate heart rates and arterial pressure. Although we did not have any clinical problems, a loss of atrioventricular conduction in infants may have clinical significance because of the contribution of atrial contraction to stroke volume. This would be particularly important if airway problems and hypoxaemia developed during an inhalation induction, or if the infant were hypovolaemic.

In summary, the use of incremental or high-concentration sevoflurane for anaesthetic induction in unpremedicated infants was associated with a 20% incidence of nodal rhythm. This unexpected finding highlights the importance of using continuous ECG analysis when studying the side effects of volatile agents in young children.


    Acknowledgements
 
We would like to thank Hertford Medical for the supply of the Recollect Dual Channel mini-Holter device.


    Footnotes
 
* Corresponding author: Department of Anaesthesia, Birmingham Children’s Hospital, Steelhouse Lane, Birmingham B4 6NH, UK Back


    References
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
1 Epstein RH, Stein AL, Marr AT, Lessin JB. High concentration versus incremental induction of anaesthesia with sevoflurane in children: a comparison of induction times, vital signs and complications. J Clin Anesth 1998; 10: 41–5[ISI][Medline]

2 Meretoja OA, Taivainene T, Raiha L, Korpela R, Wirtavuori K. Sevoflurane–nitrous oxide or halothane–nitrous oxide for paediatric bronchoscopy and gastroscopy. Br J Anaesth 1996; 76: 767–71[Abstract/Free Full Text]

3 Townsend P, Stokes MA. Bradycardia during rapid inhalation induction with sevoflurane in children. Br J Anaesth 1998; 80: 410

4 Maruyama K, Agata H, Ono K, Hiroki K, Fujihara T. Slow induction with sevoflurane was associated with complete atrioventricular block in a child with hypertension, renal dysfunction, and impaired cardiac conduction. Paediatr Anaesth 1998; 8: 73–8[ISI][Medline]

5 Southall DP, Johnston F, Shinebourne EA, Johnston PG. 24-hour electrographic study of heart rate and rhythm patterns in a population of healthy children. Br Heart J 1981; 45: 281–91[Abstract]

6 Sigston PE, Jenkins AMC, Jackson EA, Sury MRJ, Mackersie AM, Hatch DJ. Rapid inhalational induction in children: 8% sevoflurane compared with 5% halothane. Br J Anaesth 1997; 78: 362–5[Abstract/Free Full Text]

7 Blayney MR, Malins AF, Cooper GM. Cardiac arrhythmias in children during outpatient general anaesthesia for dentistry. Lancet 1999; 354: 1864–6[ISI][Medline]