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CARDIOVASCULAR RESPONSES TO ENFLURANE INDUCTION FOLLOWED BY SUXAMETHONIUM IN CHILDREN
Br. J. Anaesth. (1983), 55, 269
CARDIOVASCULAR RESPONSES TO ENFLURANE INDUCTION FOLLOWED BY SUXAMETHONIUM IN CHILDREN L . LlNDGREN AND L . SAARNIVAARA SUMMARY
Occasionally venepuncture is undesirable, or indeed impossible, in the unanaesthetized child and induction of anaesthesia with halothane, via a face-mask, is used commonly in this situation. However, enflurane may be preferable to halothane for the following reasons: the induction (Govaerts and Sanders, 1975) and recovery times (Lindgren, 1981a) are shorter in children, and serious cardiac arrhythmias are less common (Lindgren, 1981b). However, tracheal intubation under enflurane alone, without neuromuscular blockade, is associated with central nervous system excitation (Yakaitis, Blitt and Angiulo, 1979) and it would seem necessary to administer suxamethonium to permit intubation of the trachea in association with enflurane anaesthesia. There is no known contraindication to the use of suxamethonium in this situation, although the combination of halothane with suxamethonium causes cardiac arrhythmias in adults (Karhunen, Heinonen and Tammisto, 1972). In the present study, the use of enflurane, in combination with different doses of suxamethonium, was evaluated in children with special reference to the cardiovascular responses elicited.
0.03 mg kg" 1 given orally about 90 min before the induction of anaesthesia. Enflurane 5vol% was administered in 70% nitrous oxide in oxygen. A Rees modification of the Ayre's T-piece with a face-mask was used. Doubled average values for minute ventilation were used as listed in Documenta Geigy Scientific Tables (Ciba-Geigy Ltd, 1975). After the disappearance of the eyelash reflex, the possibility of performing a venepuncture was assessed every 10 s by pricking the dorsum of the hand with a needle. By the time the child was unreactive to the prick of the needle venepuncture could always be performed successfully. The time from the start of anaesthesia to the performance of venepuncture was recorded with a stop-watch. The trachea was intubated following suxamethonium 1, 1.5 or 2 mg kg" • i. v. The lungs were inflated with 100% oxygen after the suxamethonium. Systolic arterial pressure was measured indirectly with a Riva-Rocci method (detecting the pulse beat by auscultation) before the start of induction, and immediately before and after tracheal intubation. The inflatable portion of the TABLE I. Characteristics ofdifftrtnt treatment groups (mtan ± SD). Number of childrtn in partntheses
PATIENTS AND METHODS
Patients and anaesthesia The characteristics of the 58 children included in the study are shown in table I. The children were premedicated with triclofos 70 mg kg" 1 and atropine L. LINDGREN, M.D.; LAILA SAARNTVAARA, M.D.;Otolaryngolog-
ical Hospital, University of Helsinki, Haartmaninkatu 4E, SF00290 Helsinki 29, Finland. Correspondence to L.S.
Male
Weight (kg)
Age (yr)
Haemoglobin concn (g litre"1)
Suxamethonium 1 mg kg ' (19) 10 3.111.8
14.0±3.7
12618.1
Suxamethonium 1.5mgkg~' (19) 11 3.011.5
14.013.6
12718.3
Suxamethonium 2 mg kg"' (20) 14 2.511.5
13.4±3.6
12818.2
© The Macmillan Press Ltd 1983
Downloaded from http://bja.oxfordjournals.org/ at University of Michigan on June 29, 2015
Induction of anaesthesia with enflurane 5vol% plus 70% nitrous oxide in oxygen was followed by suxamethonium 1, 1.5 or 2mgkg"' i.v. and the cardiovascular changes studied in 58 children. The eyelash reflex disappeared in 44 ± 1.2 (SEM) s and the venepuncture could be performed 1.8 ± 0.05 (SEM)min after the start of enflurane anaesthesia. The increase in systolic arterial pressure after tracheal intubation was less marked after enflurane than after thiopentone (taken from an earlier study). Heart rate increased significantly after all doses of suxamethonium, but no cardiac arrhythmias were seen. The QT interval was significantly prolonged by enflurane ( P < 0.001), but remained unchanged after suxamethonium.
BRITISH JOURNAL OF ANAESTHESIA
270
RESULTS
The eyelash reflex was abolished in 44 ± 1.2 (SEM) s and venepuncture was possible 1.8 + 0.05 (SEM) min after the start of enflurane anaesthesia. Systolic arterial pressure decreased by 11.9±3.1 (SEM)mm Hg on induction of anaesthesia (fig. 1) and then increased by 12.8± 3.3 (SEM) mm Hg after intubation of the trachea. There were no significant differences in the cardiovascular responses between the different doses of suxamethonium and, therefore, all the groups were analysed together. After tracheal intubation, the mean increase in systolic arterial pressure in the enflurane group was significantly less (P<0.01) than that noted in an earlier study on thiopentone by Lindgren, Saarnivaara and Himberg (1980) (29.4 ±4 (SEM) mm Hg). The average QT interval was significantly prolonged after enflurane (469 ±5 (SEM) ms) compared with an initial value of 446 ± 6 ms ( P < 0.001) (fig. 2). In 48% of the children, the T wave became biphasic during induction with enflurane. None of the doses of suxamethonium, given after enflurane, prolonged the QT interval. The mean QT interval after laryngoscopy and tracheal intubation was similar to that obtained after induction. Heart rate decreased significantly after enflurane (137±5beatmin~1) compared with its preinduction value (146±6beatmin~') (P<0.01), whereas 30s after any of the doses of suxamethonium, heart rate had increased significantly (156 ±4 beat min"1) (P<0.001). No cardiac arrhythmias were seen
JZ U
After induction
+40
After intubation
+20
1 -20 Thiopentone
Enflurone
FIQ. 1. Changes in systolic arterial pressure immediately after induction with thiopentone 5mgkg~' or enflurane 5vol% plus 70%'nitrous oxide in oxygen, and following tracheal intubation facilitated with suxamethonium. Mean values for 21 to 58 children. Bars indicate SEM. Results for the thiopentone group from a previous study (Lindgren, Saarnivaara and Himberg, 1980). Doses of suxamethonium: after thiopentone l.Smgkg" 1 ; after enflurane 1,1.5 or 2mgkg~' i.v. Initial values ranged from 90 to 130mmHg. *P<0.01 for the difference between the thiopentone group and the enflurane group.
either after induction with enflurane or following any of the doses of suxamethonium. DISCUSSION
The present study shows that the induction of anaesthesia with enflurane in combination with suxamethonium could be useful in young children with difficult veins. No cardiac arrhythmias were noted with this combination and the increase in systolic arterial pressure on tracheal intubation was less marked than after thiopentone (Lindgren, Saarnivaara and Himberg, 1980). Cardiovascular responses
The increase in systolic arterial pressure on intubation was less marked in the present study than that noted previously by Lindgren, Saarnivaara and Himberg (1980) with thiopentone. Barbiturates do not depress laryngeal reflexes (Goodman and Gilman, 1975) and, therefore, enflurane may provide more adequate anaesthesia for laryngeal and trache-
Downloaded from http://bja.oxfordjournals.org/ at University of Michigan on June 29, 2015
arterial pressure cuff completely encircled the upper arm and the cuff extended for two-thirds of the I length equidistant between the shoulder and elbow. £ +io For comparison, similar data for thiopentone were taken from an earlier study (Lindgren, Saarnivaara and Himberg, 1980). Heart rate and the ECG (lead in — AVR) with three surface electrodes were dis- in played continuously on an oscilloscope and a con- cL +20 tinuous record of the ECG obtained. Monitoring was started 1 min before induction of anaesthesia HI and discontinued 5 min after trachea! intubation. QT intervals were measured before and after induction, 30 s after suxamethonium, after laryngoscopy and after intubation as described by Lindgren (1981b). All the children were anaesthetized by the in same anaesthetist (L.L.). Student's t tests for paired and unpaired data were -20 used for the statistical analysis of the results. O
ENFLURANE INDUCTION IN CHILDREN
271 170
480r
_
470
rfi
in
jE
I
— 460 a 450 O
uo
Init.
rh
I i
£ I i
Enfl.
QT interval
L
Sux.
Lar.
160
c
150
g
140
130
g
Int.
Heart rate
FIG. 2. QT intervals (ms) and heart rate (beat min ) during the induction of anaesthesia. Mean values ±SEM for 58 children. Init. - Initial value; Enfl. = 1.8 ± 0.4{SD) min after inhalation of enflurane 5 vol% plus 70% nitrous oxide in oxygen; Sux. = 30s after injection of suxamethonium 1, l.S or 2mgkg~ 1 i.v.; Lar. = After laryngoscopy; Int.- After intubation. *P<0.001 from initial QT interval; • =P<0.01; • • = P<0.001 from preceding heart rate.
al manipulation than thiopentone. No cardiac arrhythmias were seen in this study although heart rate increased significantly after all doses of suxamethonium. Low doses of suxamethonium stimulate cardiac cholinergic receptors and cause bradycardia, whereas larger doses stimulate cardiac sympathetic ganglia and result, indirectly, in tachycardia (Goat, 1972). Since halothane depresses the sympathetic nervous system (Skovsted, Price and Price, 1969), bradycardia occurs after small doses of suxamethonium in the presence of halothane (Karhunen, Heinonen and Tammisto, 1972) and since halothane sensitizes the heart to the arrhythmogenic effect of catecholamines (Katz and Katz, 1966) ectopic rhythms may occur after larger doses of suxamethonium in the presence of halothane. The present results support an earlier observation by Reisner and Lippman (1975) in adults, and that obtained by Lindgren (1981b) in children, that enflurane has antiarrhythmic properties. Since cardiac arrhythmias can occur after suxamethonium in the presence of halothane, we feel that this combination cannot be recommended. However, halothane without suxamethonium produces ideal conditions for intubation (Yakaitis, Blitt and Angiulo, 1979). The QT interval was significantly prolonged after
enflurane, a feature also noted by Lindgren (1981b), but did not change further after suxamethonium and no cardiac arrhythmia a occurred. In an earlier study (Saarnivaara and Lindgren, 1980) the QT interval was significantly prolonged after thiopentone and the most marked prolongation occurred after suxamethonium and ventricular ectopic beats occurred in 22% of the children studied. The relationship between the prolongation of the QT interval and cardiac arrhythmia is complicated. There are anti-arrhythmic drugs like quinidine which prolong the QT interval. Quinidine increases the diastolic electrical current threshold as well as the fibrillation threshold in atrial and ventricular muscles and in Purkinje fibres (Wallace et al., 1966). On the other hand, Ahnve, Lundman and Shoaleh-var (1978) found that prolongation of the QT interval in acute myocardial infarction was associated with ventricular arrhythmia. Moreover, there are patients who suffer from congenitally prolonged QT intervals, syncopal attacks resulting from ventricular fibrillation and increasing the likelihood of sudden death (Jervell and Lange-Nielsen, 1957; Romano, Gemme and Pongiglione, 1963; Ward, 1964). In these patients, the prolongation of the QT interval may be caused by an imbalance in the cardiac sympathetic tone. This suggestion is based
Downloaded from http://bja.oxfordjournals.org/ at University of Michigan on June 29, 2015
4i
rh
BRITISH JOURNAL OF ANAESTHESIA
272
ACKNOWLEDGEMENT
We wish to thank the nunes working in anaesthesia for their skilful assistance during this study.
REFERENCES
Ahnve, S., Lundman, T., and Shoaleh-var, M. (1978). The relationship between QT interval and ventricular arrhythmias in acute mybcardial infarction. Acta Mtd. Scand., 204,17. Ciba-Geigy Ltd (1975). Documenta Geigy, Scientific Tables, 7th edn, p. 550. Basel: Ciba-Geigy Ltd. Galindo, A., and Davis, T. (1962). Succinylcholine and cardiac excitability. Anesthtsiology, 23, 32. Goat, V. A. (1972). The effect of succinylcholine on the isolated mammalian heart. Proc. R. Soc. Med.,65, 149. Goodman, L. S., and Gilman, A. (1975). The Pharmacological Basis of Therapeutics, 5th edn, p. 109. New York, Toronto and London: Macmillan. Govaerts, M. J., and Sanders, M.(1975). Induction and recovery with enflurane and halothane in paediatric anaesthesia. Br. J. Anaesth., AT, 877.
Gothert, M., and Wendt, J. (1977). Inhibition of adrenal medullary catecholamine secretion by enflurane. I. Investigations in moo. Anesthtsiology, 46, 400. Jervell, A., and Lange-Nielsen, F. (1957). Congenital deafmutism, functional heart diiease, with prolongation of the Q-T interval and sudden death. Am. Heart J., 54, 59. Karhunen, U., Heinonen, J., and Tammisto, T. (1972). The effect of tubocurarine and alcuronium or suxamethoniuminduced change* in cardiac rate and rhythm. Ada Anaesthesiol. Scand., 16, 3. Katz, R.L., and Katz.G.J. (1966). Surgical infiltration of pressor drugs and their interactions with volatile anaesthetics. Br. J. Anaesth., 38,712. Lindgren, L. (1981a). Comparison of halothane and enflurane anaesthesia for otolaryngological surgery in children. Br. J. Anaesth., 53, 537. (1981b). E.c.g. changes during halothane and enflurane anaesthesia for ENT surgery in children. Br. J. Anaesth., 53, 653.
Lindgren, L., Saarnivaara, L., and Himberg, J.-J. (1980). Comparison of oral triclofos, diazepam and flunitrazepam as premedicants in children undergoing otolaryngological surgery. Br.]. Anaesth., S2, 283. Lupprian, K. G., and Churchill-Davidson, H. D. (1960). Effect of suxamethonium on cardiac rhythm. Br. Mtd. J., 2, 1774. Moss, A. J., and McDonald, J. (1971). Unilateral cervicothoracic sympathetic ganglionectomy for the treatment of long QTinterval syndrome. N. Engl. J. Mtd., 285,903. Olley, D. M., and Fowler, R. S. (1970). The surdocardiac syndrome and therapeutic observations. Br. Heart. J., 32,467. Reisner, L., and Lippman, M. (1975). Ventricular arrhythmia* after epinephrine injection in enflurane and in halothane anesthesia. Antsth. Analg., 54, 468. Romano, C , Gemme, G., and Pongiglione, R. (1963). Aritmie cardiache rare dell'eta pediatrics II. Accessi sincopali per fibrillazione ventricolare par ossistica. Clin. Pediatr. (Bologna), 45, 656. Saarnivaara, L., and Lindgren, L. (1980). Prolongation of the QT interval during induction of anaesthesia. 7th World Congress of Anaesthesiologists Hamburg, F.R.G. International Congress Series No. 533, 570. Skovsted, P., Price, M. L., and Price, H. L. (1969). The effects of halothane on arterial pressure, preganglionic sympathetic activity and barostatic reflexes. Anesthtsiology, 31, 507. Wallace, A. G.,Cline, R. E., Sealy, W. C , Young, W.G. jr,and Troyer, W. G. jr (1966). Electrophysiologic effects of quinidine. Studies using chronically implanted electrodes in awake dogs with and without cardiac denervation. Circ. Rts., 19,960. Ward, O. C. (1964). A new familial cardiac syndrome in children. / . Irish Mtd. Assoc., 54, 103. Yakaitis, R. W., Blitt, C. D., and Angiulo, J. P. (1979). Endtidal enflurane concentration for endotracheal intubation. Anesthesiology, 50, 59.
REPONSES CARDIO-VASCULAIRES A L'lNDUCTION A L'ENFLURANE SUTVIE DE SUXAMETHONIUM CHEZ L'ENFANT RESUME
L'induction de l'anesthesie par l'enflurane 5 vol% plus le protoxyde d'azote 70% dans l'oxygene a et£ suivie de l'injection i. v. de 1, 1,5, 2mgkg~' de suxamethonium, et on a 6tudi£ les modifications cardiovasculaires chez 58 enfants. Le rfflexe du clignement disparaissait en 49 ± 1,2 (ES) s et la ponction veineuse
Downloaded from http://bja.oxfordjournals.org/ at University of Michigan on June 29, 2015
on the facts that these patients have been successfully treated with a 0-adrenergic receptor blocking agent (Olley and Fowler, 1970) and that blockade of the left stellate ganglion was performed (Moss and McDonald, 1971). Suxamethonium stimulates both the parasympathetic and the sympathetic nervous system (Lupprian and Churchill-Davidson, 1960; Galindo and Davis, 1962; Goat, 1972). Therefore, prolongation of the QT interval after suxamethonium in anaesthesia induced with thiopentone may be an imbalance in the cardiac sympathetic tone induced with suxamethonium. Hence, the decrease in sympathetic activity associated with enflurane (Gothert and Wendt, 1977) may prevent the prolongation of the QT interval after suxamethonium as well as cardiac arrhythmia.
ENFLURANE INDUCTION IN CHILDREN
273
KARDIOVASKULARE REAKTIONEN AUF ENFLURANE-EINLEITUNG UND DARAUFFOLGENDER SUXAMETHONIUMGABE BEI KINDERN
RESPtJESTAS CARDIOVASCULARES A LA INDUCCI6N POR ENFLURANO SEGUIDO POR SUXAMETONIO EN NINOS
ZUSAMMENFASSUNG
Se Uevo a cabo un estudio de la inducci6n de la anestesia por enflurano al 5 vol% atirmi* de oxido nitroso en ozigeno al 70%, seguido por 1, 1,3 6 2mgkg~' i.v. de suzametonio y de los cam bios cardiovasculares prorocados en 38 ninos. El rcflejo de las pestanas desaparecid en 44 ± 1,2 (SEM) s y la venepunctura pudo reauzane 1,8 ±0,05 (SEM) min despuet del principio de la anestesia por enflurano. El aumento de la presi6n arterial aist61ica despues de la intubacidn traqueal fue menos marcado dcspues del enflurano que despues de la tiopentona (segun un estudio previo). El ritmo cardiaco aumentd de manera significante despues de todas las dosis de suzametonio, pero no se obsemS arritmia cardiacs alguna. El intervalo QT fue prolongado de manera significariva por el enflurano (P<0,001), pero se mantuvo sin cambio despues del suzametonio.
SUMAJUO
Downloaded from http://bja.oxfordjournals.org/ at University of Michigan on June 29, 2015
Bd 58 Kindern wurde nach einer Narkosccinleitung mit 5 Vol% Enflurane und 70% Lachgai mit Sauerstoff 1,1,3 oder 2 mg kg"' Suzamcthonium gegeben. Die kardiovaskularen Verfinderungen wurden untersucht. Der Lidreflex verschwand nach 44 ± 1,2 (Standardfehkr) Sekunden und die Venenpunktion konnte 1,8±0,05 (Standardfehler) Minuten nach Beginn der Enfhiranenarkose vorgenommen werden. Der Anstieg des tyttolischen arteriellen Blutdrucks nach der trachealen Intubation war nach Enflurane weniger ausgepragt als nach Thiopentone (aus rinw fruheren Studie). Die Herzfrequenz stieg nftch jeder Dosis von Suzamethonium irignifikantan, jedoch waren keine Arrhythmiwi zu beobachten. Das QT-Intervall wurde durch Enflurane significant (P<0,001) verlangert, blieb jedoch durch Suzamethonium unbccinflufit.
CARDIOVASCULAR RESPONSES TO ENFLURANE INDUCTION FOLLOWED BY SUXAMETHONIUM IN CHILDREN L . LlNDGREN AND L . SAARNIVAARA SUMMARY
Occasionally venepuncture is undesirable, or indeed impossible, in the unanaesthetized child and induction of anaesthesia with halothane, via a face-mask, is used commonly in this situation. However, enflurane may be preferable to halothane for the following reasons: the induction (Govaerts and Sanders, 1975) and recovery times (Lindgren, 1981a) are shorter in children, and serious cardiac arrhythmias are less common (Lindgren, 1981b). However, tracheal intubation under enflurane alone, without neuromuscular blockade, is associated with central nervous system excitation (Yakaitis, Blitt and Angiulo, 1979) and it would seem necessary to administer suxamethonium to permit intubation of the trachea in association with enflurane anaesthesia. There is no known contraindication to the use of suxamethonium in this situation, although the combination of halothane with suxamethonium causes cardiac arrhythmias in adults (Karhunen, Heinonen and Tammisto, 1972). In the present study, the use of enflurane, in combination with different doses of suxamethonium, was evaluated in children with special reference to the cardiovascular responses elicited.
0.03 mg kg" 1 given orally about 90 min before the induction of anaesthesia. Enflurane 5vol% was administered in 70% nitrous oxide in oxygen. A Rees modification of the Ayre's T-piece with a face-mask was used. Doubled average values for minute ventilation were used as listed in Documenta Geigy Scientific Tables (Ciba-Geigy Ltd, 1975). After the disappearance of the eyelash reflex, the possibility of performing a venepuncture was assessed every 10 s by pricking the dorsum of the hand with a needle. By the time the child was unreactive to the prick of the needle venepuncture could always be performed successfully. The time from the start of anaesthesia to the performance of venepuncture was recorded with a stop-watch. The trachea was intubated following suxamethonium 1, 1.5 or 2 mg kg" • i. v. The lungs were inflated with 100% oxygen after the suxamethonium. Systolic arterial pressure was measured indirectly with a Riva-Rocci method (detecting the pulse beat by auscultation) before the start of induction, and immediately before and after tracheal intubation. The inflatable portion of the TABLE I. Characteristics ofdifftrtnt treatment groups (mtan ± SD). Number of childrtn in partntheses
PATIENTS AND METHODS
Patients and anaesthesia The characteristics of the 58 children included in the study are shown in table I. The children were premedicated with triclofos 70 mg kg" 1 and atropine L. LINDGREN, M.D.; LAILA SAARNTVAARA, M.D.;Otolaryngolog-
ical Hospital, University of Helsinki, Haartmaninkatu 4E, SF00290 Helsinki 29, Finland. Correspondence to L.S.
Male
Weight (kg)
Age (yr)
Haemoglobin concn (g litre"1)
Suxamethonium 1 mg kg ' (19) 10 3.111.8
14.0±3.7
12618.1
Suxamethonium 1.5mgkg~' (19) 11 3.011.5
14.013.6
12718.3
Suxamethonium 2 mg kg"' (20) 14 2.511.5
13.4±3.6
12818.2
© The Macmillan Press Ltd 1983
Downloaded from http://bja.oxfordjournals.org/ at University of Michigan on June 29, 2015
Induction of anaesthesia with enflurane 5vol% plus 70% nitrous oxide in oxygen was followed by suxamethonium 1, 1.5 or 2mgkg"' i.v. and the cardiovascular changes studied in 58 children. The eyelash reflex disappeared in 44 ± 1.2 (SEM) s and the venepuncture could be performed 1.8 ± 0.05 (SEM)min after the start of enflurane anaesthesia. The increase in systolic arterial pressure after tracheal intubation was less marked after enflurane than after thiopentone (taken from an earlier study). Heart rate increased significantly after all doses of suxamethonium, but no cardiac arrhythmias were seen. The QT interval was significantly prolonged by enflurane ( P < 0.001), but remained unchanged after suxamethonium.
BRITISH JOURNAL OF ANAESTHESIA
270
RESULTS
The eyelash reflex was abolished in 44 ± 1.2 (SEM) s and venepuncture was possible 1.8 + 0.05 (SEM) min after the start of enflurane anaesthesia. Systolic arterial pressure decreased by 11.9±3.1 (SEM)mm Hg on induction of anaesthesia (fig. 1) and then increased by 12.8± 3.3 (SEM) mm Hg after intubation of the trachea. There were no significant differences in the cardiovascular responses between the different doses of suxamethonium and, therefore, all the groups were analysed together. After tracheal intubation, the mean increase in systolic arterial pressure in the enflurane group was significantly less (P<0.01) than that noted in an earlier study on thiopentone by Lindgren, Saarnivaara and Himberg (1980) (29.4 ±4 (SEM) mm Hg). The average QT interval was significantly prolonged after enflurane (469 ±5 (SEM) ms) compared with an initial value of 446 ± 6 ms ( P < 0.001) (fig. 2). In 48% of the children, the T wave became biphasic during induction with enflurane. None of the doses of suxamethonium, given after enflurane, prolonged the QT interval. The mean QT interval after laryngoscopy and tracheal intubation was similar to that obtained after induction. Heart rate decreased significantly after enflurane (137±5beatmin~1) compared with its preinduction value (146±6beatmin~') (P<0.01), whereas 30s after any of the doses of suxamethonium, heart rate had increased significantly (156 ±4 beat min"1) (P<0.001). No cardiac arrhythmias were seen
JZ U
After induction
+40
After intubation
+20
1 -20 Thiopentone
Enflurone
FIQ. 1. Changes in systolic arterial pressure immediately after induction with thiopentone 5mgkg~' or enflurane 5vol% plus 70%'nitrous oxide in oxygen, and following tracheal intubation facilitated with suxamethonium. Mean values for 21 to 58 children. Bars indicate SEM. Results for the thiopentone group from a previous study (Lindgren, Saarnivaara and Himberg, 1980). Doses of suxamethonium: after thiopentone l.Smgkg" 1 ; after enflurane 1,1.5 or 2mgkg~' i.v. Initial values ranged from 90 to 130mmHg. *P<0.01 for the difference between the thiopentone group and the enflurane group.
either after induction with enflurane or following any of the doses of suxamethonium. DISCUSSION
The present study shows that the induction of anaesthesia with enflurane in combination with suxamethonium could be useful in young children with difficult veins. No cardiac arrhythmias were noted with this combination and the increase in systolic arterial pressure on tracheal intubation was less marked than after thiopentone (Lindgren, Saarnivaara and Himberg, 1980). Cardiovascular responses
The increase in systolic arterial pressure on intubation was less marked in the present study than that noted previously by Lindgren, Saarnivaara and Himberg (1980) with thiopentone. Barbiturates do not depress laryngeal reflexes (Goodman and Gilman, 1975) and, therefore, enflurane may provide more adequate anaesthesia for laryngeal and trache-
Downloaded from http://bja.oxfordjournals.org/ at University of Michigan on June 29, 2015
arterial pressure cuff completely encircled the upper arm and the cuff extended for two-thirds of the I length equidistant between the shoulder and elbow. £ +io For comparison, similar data for thiopentone were taken from an earlier study (Lindgren, Saarnivaara and Himberg, 1980). Heart rate and the ECG (lead in — AVR) with three surface electrodes were dis- in played continuously on an oscilloscope and a con- cL +20 tinuous record of the ECG obtained. Monitoring was started 1 min before induction of anaesthesia HI and discontinued 5 min after trachea! intubation. QT intervals were measured before and after induction, 30 s after suxamethonium, after laryngoscopy and after intubation as described by Lindgren (1981b). All the children were anaesthetized by the in same anaesthetist (L.L.). Student's t tests for paired and unpaired data were -20 used for the statistical analysis of the results. O
ENFLURANE INDUCTION IN CHILDREN
271 170
480r
_
470
rfi
in
jE
I
— 460 a 450 O
uo
Init.
rh
I i
£ I i
Enfl.
QT interval
L
Sux.
Lar.
160
c
150
g
140
130
g
Int.
Heart rate
FIG. 2. QT intervals (ms) and heart rate (beat min ) during the induction of anaesthesia. Mean values ±SEM for 58 children. Init. - Initial value; Enfl. = 1.8 ± 0.4{SD) min after inhalation of enflurane 5 vol% plus 70% nitrous oxide in oxygen; Sux. = 30s after injection of suxamethonium 1, l.S or 2mgkg~ 1 i.v.; Lar. = After laryngoscopy; Int.- After intubation. *P<0.001 from initial QT interval; • =P<0.01; • • = P<0.001 from preceding heart rate.
al manipulation than thiopentone. No cardiac arrhythmias were seen in this study although heart rate increased significantly after all doses of suxamethonium. Low doses of suxamethonium stimulate cardiac cholinergic receptors and cause bradycardia, whereas larger doses stimulate cardiac sympathetic ganglia and result, indirectly, in tachycardia (Goat, 1972). Since halothane depresses the sympathetic nervous system (Skovsted, Price and Price, 1969), bradycardia occurs after small doses of suxamethonium in the presence of halothane (Karhunen, Heinonen and Tammisto, 1972) and since halothane sensitizes the heart to the arrhythmogenic effect of catecholamines (Katz and Katz, 1966) ectopic rhythms may occur after larger doses of suxamethonium in the presence of halothane. The present results support an earlier observation by Reisner and Lippman (1975) in adults, and that obtained by Lindgren (1981b) in children, that enflurane has antiarrhythmic properties. Since cardiac arrhythmias can occur after suxamethonium in the presence of halothane, we feel that this combination cannot be recommended. However, halothane without suxamethonium produces ideal conditions for intubation (Yakaitis, Blitt and Angiulo, 1979). The QT interval was significantly prolonged after
enflurane, a feature also noted by Lindgren (1981b), but did not change further after suxamethonium and no cardiac arrhythmia a occurred. In an earlier study (Saarnivaara and Lindgren, 1980) the QT interval was significantly prolonged after thiopentone and the most marked prolongation occurred after suxamethonium and ventricular ectopic beats occurred in 22% of the children studied. The relationship between the prolongation of the QT interval and cardiac arrhythmia is complicated. There are anti-arrhythmic drugs like quinidine which prolong the QT interval. Quinidine increases the diastolic electrical current threshold as well as the fibrillation threshold in atrial and ventricular muscles and in Purkinje fibres (Wallace et al., 1966). On the other hand, Ahnve, Lundman and Shoaleh-var (1978) found that prolongation of the QT interval in acute myocardial infarction was associated with ventricular arrhythmia. Moreover, there are patients who suffer from congenitally prolonged QT intervals, syncopal attacks resulting from ventricular fibrillation and increasing the likelihood of sudden death (Jervell and Lange-Nielsen, 1957; Romano, Gemme and Pongiglione, 1963; Ward, 1964). In these patients, the prolongation of the QT interval may be caused by an imbalance in the cardiac sympathetic tone. This suggestion is based
Downloaded from http://bja.oxfordjournals.org/ at University of Michigan on June 29, 2015
4i
rh
BRITISH JOURNAL OF ANAESTHESIA
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ACKNOWLEDGEMENT
We wish to thank the nunes working in anaesthesia for their skilful assistance during this study.
REFERENCES
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REPONSES CARDIO-VASCULAIRES A L'lNDUCTION A L'ENFLURANE SUTVIE DE SUXAMETHONIUM CHEZ L'ENFANT RESUME
L'induction de l'anesthesie par l'enflurane 5 vol% plus le protoxyde d'azote 70% dans l'oxygene a et£ suivie de l'injection i. v. de 1, 1,5, 2mgkg~' de suxamethonium, et on a 6tudi£ les modifications cardiovasculaires chez 58 enfants. Le rfflexe du clignement disparaissait en 49 ± 1,2 (ES) s et la ponction veineuse
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on the facts that these patients have been successfully treated with a 0-adrenergic receptor blocking agent (Olley and Fowler, 1970) and that blockade of the left stellate ganglion was performed (Moss and McDonald, 1971). Suxamethonium stimulates both the parasympathetic and the sympathetic nervous system (Lupprian and Churchill-Davidson, 1960; Galindo and Davis, 1962; Goat, 1972). Therefore, prolongation of the QT interval after suxamethonium in anaesthesia induced with thiopentone may be an imbalance in the cardiac sympathetic tone induced with suxamethonium. Hence, the decrease in sympathetic activity associated with enflurane (Gothert and Wendt, 1977) may prevent the prolongation of the QT interval after suxamethonium as well as cardiac arrhythmia.
ENFLURANE INDUCTION IN CHILDREN
273
KARDIOVASKULARE REAKTIONEN AUF ENFLURANE-EINLEITUNG UND DARAUFFOLGENDER SUXAMETHONIUMGABE BEI KINDERN
RESPtJESTAS CARDIOVASCULARES A LA INDUCCI6N POR ENFLURANO SEGUIDO POR SUXAMETONIO EN NINOS
ZUSAMMENFASSUNG
Se Uevo a cabo un estudio de la inducci6n de la anestesia por enflurano al 5 vol% atirmi* de oxido nitroso en ozigeno al 70%, seguido por 1, 1,3 6 2mgkg~' i.v. de suzametonio y de los cam bios cardiovasculares prorocados en 38 ninos. El rcflejo de las pestanas desaparecid en 44 ± 1,2 (SEM) s y la venepunctura pudo reauzane 1,8 ±0,05 (SEM) min despuet del principio de la anestesia por enflurano. El aumento de la presi6n arterial aist61ica despues de la intubacidn traqueal fue menos marcado dcspues del enflurano que despues de la tiopentona (segun un estudio previo). El ritmo cardiaco aumentd de manera significante despues de todas las dosis de suzametonio, pero no se obsemS arritmia cardiacs alguna. El intervalo QT fue prolongado de manera significariva por el enflurano (P<0,001), pero se mantuvo sin cambio despues del suzametonio.
SUMAJUO
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Bd 58 Kindern wurde nach einer Narkosccinleitung mit 5 Vol% Enflurane und 70% Lachgai mit Sauerstoff 1,1,3 oder 2 mg kg"' Suzamcthonium gegeben. Die kardiovaskularen Verfinderungen wurden untersucht. Der Lidreflex verschwand nach 44 ± 1,2 (Standardfehkr) Sekunden und die Venenpunktion konnte 1,8±0,05 (Standardfehler) Minuten nach Beginn der Enfhiranenarkose vorgenommen werden. Der Anstieg des tyttolischen arteriellen Blutdrucks nach der trachealen Intubation war nach Enflurane weniger ausgepragt als nach Thiopentone (aus rinw fruheren Studie). Die Herzfrequenz stieg nftch jeder Dosis von Suzamethonium irignifikantan, jedoch waren keine Arrhythmiwi zu beobachten. Das QT-Intervall wurde durch Enflurane significant (P<0,001) verlangert, blieb jedoch durch Suzamethonium unbccinflufit.