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E.C.G. CHANGES DURING HALOTHANE AND ENFLURANE ANAESTHESIA FOR E.N.T. SURGERY IN CHILDREN
Br. J. Anaesth. (1981), 53, 653
E.C.G. CHANGES DURING HALOTHANE AND ENFLURANE ANAESTHESIA FOR E.N.T. SURGERY IN CHILDREN L. LlNDGREN SUMMARY
Oral surgery under general anaesthesia may provoke serious cardiac arrhythmia (Kaufman, 1965; Tuohy, 1968), often initiated as a reflex caused by the stimulation of the pharynx and trachea (Katz and Bigger, 1970). Halothane is associated with a high frequency of arrhythmia during oral surgery (Tuohy, 1968; Fisch et al., 1969; Saarnivaara et al., 1974; Gotta et al., 1976). Atlee and Rusy (1972,1977) have shown that halothane prolongs A-V nodal, His-Purkinje and ventricular conduction, whereas enflurane only prolongs A-V nodal conduction in dogs. They concluded that conduction changes such as occur with halothane are necessary for ventricular arrhythmias caused by re-entry of excitation and that enflurane is less likely to cause these arrhythmias. Thiopentone appears to increase aberrant ventricular conduction in patients with Wolf-Parkinson-White syndrome (Kadis and Gianelly, 1973). Cundy (1973) has reported a case in which the administration of Althesin effectively abolished ventricular ectopic beats. Alexander (1974) and Saarnivaara and Kentala (1977) found that Althesin protected against ventricular arrhythmia during oral surgery. Prolongation of the QT interval in e.c.g. is a sign of imbalance in cardiac sympathetic activity LEENA
LINDGREN,
M.D.,
Otolaryngological
Hospital,
University of Helsinki, Haartmaninkatu 4E, SF-00290 Helsinki 29, Finland. 0007-0912/81/060653-10 801.00
(Schwartz, Stone and Brown, 1976). This is associated with ventricular arrhythmia in acute myocardial infarction (Ahnve, Lundman and Shoaleh-var, 1978) and is a predictor of sudden death in this disease (Schwartz and Wolf, 1978). Wig and others (1979) have described sudden cardiac arrest in a patient with a prolonged QT interval during halothane anaesthesia. Kentala and Repo (1979) found a prolonged QT interval during exercise testing to be of prognostic value in relation to survival after acute myocardial infarction. The present study was designed to compare the frequency of cardiac arrhythmia during halothane or enflurane anaesthesia, after induction with thiopentone or Althesin, in children undergoing e.n.t. surgery. The effect of anaesthetics on QT intervals was studied and the changes in QT intervals in association with cardiac arrhythmia were evaluated. PATIENTS AND METHODS
One hundred and fifty-two unselected children, with no cardiac disease, undergoing adenoidectomy or adenotonsillectomy (T + A) were studied (table I). Anaesthesia
Premedication was triclofos 70mgkg~' and atropine 0.03mgkg" 1 given orally about 90min before the start of anaesthesia. A needle was inserted to the left cubital vein. In the adenoidectomy group, 45 children were anaes© Macmillan Publishers Ltd 1981
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E.c.g. changes were compared in 152 children undergoing adenoidectomy or adenotonsillectomy ( T +A) under halothane or enflurane anaesthesia. Junctional rhythm occurred in 4-16% of the children in adenoidectomy groups and in 11-33% in T + A groups. Bundle branch block occurred in 4% of the children anaesthetized with halothane, but not with enflurane and was particularly common in association with thiopentone and T + A operations; one patient had bifocal ventricular tachycardia. QT interval was prolonged compared with control after thiopentone (P<0.001) and thiopentone and suxamethonium (P<0.02). QT interval was not changed after Althesin with or without suxamethonium. Mean preanaesthetic QT interval ( ± SEM) was significantly prolonged (492 ± 22 ms; normal 440 ms) in children showing aberrant conduction with chaotic rhythm, but normal (438 ± 5 ms) when bundle branch block or junctional rhythm was present during halothane anaesthesia. QT interval was prolonged significantly in enflurane but not in halothane anaesthesia.
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TABLE I. Sex, age, weight and haemoglobin concentration in different treatment groups. Mean value +_ SD. Number of children in parentheses
(yr)
Weight (kg)
Haemoglobin (gUtre"')
14 14
4.1 ±2.6 4.7±2.3
17.7±7.6 17.5±4.7
135±7.2 136±9.0
17
7.2±2.8
25.6±9.6
124±8.0
15 14
4.3±2.7 4.9±2.5
18.2±6.5 18.5±5.8
135±9.4 132±7.0
15
6.4±2.7
22.7±8.1
127±8.2
Age
Halothane Adenoidectomy Thiopentone (20) Althesin (25) T +A Thiopentone (27) Enflurane Adenoidectomy Thiopentone (25) Althesin (27) T +A Thiopentone (27)
thetized with halothane (induction with thiopentone 5mgkg~' in 20, Althesin 0.06ml kg"' in 25) and 53 with enflurane (25 and 28). In the T + A group, 27 children were anaesthetized with halothane and 27 with enflurane, in either case following thiopentone 5mgkg"' and suxamethonium l.Smgkg" 1 i.v. The trachea was intubated. Mean delivered concentration of halothane was 1.1 (v/v) and of enflurane 2.0. Both anaesthetics were administered in 70% nitrous oxide in oxygen. A Rees system was used for children weighing less than 25 kg and a circle system with carbon dioxide absorption for the remainder. Ventilation of the lungs was usually controlled, but in a few patients it was assisted. End-tidal carbon dioxide concentration was kept at 5.5-6%. All the children were anaesthetized by the author. The mean duration (+ SD) of anaesthesia for adenoidectomy was 31 +_ 7 min and that of the operation 20+ 7 min. The corresponding figures for T + A were 35 ± 9 min and 24 + 8 min, respectively.
according to the following system. If the P wave preceded the QRS complex and PQ interval was shorter than 0.12 s, the junctional rhythm was considered to be upper junctional. If the P wave was hidden within the QRS complex or if it followed the QRS complex, then the junctional rhythm was considered to be middle or lower junctional, respectively (Saarnivaara and Kentala, 1977). E.cg. changes occurring before the start of inhalation anaesthesia are excluded from this study. QT intervals were measured before the induction of anaesthesia, after laryngoscopy, after intubation, 3 min after the start of the inhalation anaesthesia, after adenoidectomy or T + A and after extubation. From the e.cg. (paper speed 25mms~ 1 ) the QT interval was measured from the onset of QRS complex to the end of the T wave. The mean of four successive beats was determined. Rate correction was made according to the formula: QTC = QT/V(R-R') (Bazett, 1920). QT values exceeding 440 ms were denned as prolonged. To analyse the effects of the induction agents on QT interval, QT intervals were measured Assessment of e.cg. changes and QT interval immediately before and after venepuncture, 45 s Heart rate and the e.cg lead-AVR with three after the i.v. anaesthetic, 30 s after suxamesurface electrodes were displayed continuously on thonium, after laryngoscopy and after intubation. an oscilloscope (Mode 280, Kone Osakeyhtio, Mean age, weight and preanaesthetic QT interval Espoo, Finland) and the e.cg. was recorded. (+ SD) of the children in the thiopentone group Monitoring was started 1 min before the insertion were 5.3 ±0.5 yr, 18.8 + 1.3kg and 432±4 ms and of an i.v. cannula and discontinued 2 min after in the Althesin group 4.6 ± 0.6 yr, 18.5 ± 1.4 kg and extubation. 423 ± 4 ms. The e.cg. recordings were analysed with special Student's t tests for paired and unpaired data reference to bundle branch block and aberrant conduction. Junctional rhythm was classified were used for the statistical analysis of the results.
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Male
CARDIAC ARRHYTHMIA IN CHILDREN RESULTS
The mean preanaesthetic QT intervals ( + SD) ranged from 425 ±39 to 447 +37 ms in different groups. There was no disturbance in the e.c.g. i min before venepuncture. Table II shows that junctional rhythm occurred in 4-16% of the children in the adenoidectomy groups. In the T + A groups, the frequency of junctional rhythm ranged from 11 % to 33%. The frequency of upper and middle junctional rhythms was similar in each group.
655
477 ± 14 ms. In the children treated with lignocaine the mean pretreatment (±SEM) QT interval was 509 +24 ms and decreased significantly after lignocaine, followed by sinus rhythm (437 ± 9.7 ms)(P< 0.05). The T wave became biphasic in 15-41% of the children anaesthetized with enflurane and in 0-8 % anaesthetized with halothane. A typical example of T wave becoming biphasic is shown in figure 1. The arterial pressure was maintained during all types of e.c.g. changes.
QRS complex changes Junctional rhythm
Halothane Adenoidectomy Thiopentone (20) Althesin (25)
Upper
Middle
BBB
BBB + aberrant conduction
Biphasic T-wave
5 16
5 16
0 4
10 4
0 8
30
33
4
11
0
12 4
12 7
0 0
0 0
32** 41**
11
15
0
0
15*
T +A Thiopentone (27) Enflurane Adenoidectomy Thiopentone (25) Althesin (27) T+A Thiopentone (27)
Neither bundle branch block (BBB) nor BBB plus aberrant conduction was seen during enflurane anaesthesia, whereas the frequency of BBB ranged from 0% to 4% and BBB plus aberrant conduction was seen in six children in the halothane groups. Aberrant conduction was always associated with the surgical manipulation. In addition to the results shown in table II, one child in the Althesin plus halothane group developed BBB with aberrant conduction before the start of spontaneous breathing when the endtidal carbon dioxide was 9.5%, but this disappeared after breathing 100% oxygen. In three children BBB and aberrant conduction disappeared without treatment. In the remaining three children, e.c.g. became chaotic and this lasted more than 5 min. Administration of lignocaine lmgkg" 1 i.v. promptly abolished the arrhythmia. The mean duration (+ SEM) of QT interval during BBB with aberrant conduction was
Figure 2 shows that the mean preanaesthetic QT interval was significantly longer (492 ± 22 ms) in the children showing BBB plus aberrant conduction than in the children without e.c.g. changes (426±5.2ms) (P<0.01) and in the children with junctional rhythm or BBB (438 ± 5.3 ms) (P<0.05). Figure 3 shows the e.c.g. changes of a healthy 9-yr-old boy undergoing T + A with halothane anaesthesia. Preanaesthetic QT interval was 594 ms. During the dissection of the left tonsil there wag aberrant conduction with chaotic rhythm which resulted in bifocal ventricular tachycardia. A regular supraventricular rhythm was restored after injection of lignocaine lmgkg" 1 i.v. and sinus rhythm followed. This boy's QT interval was checked 1 year later after a normal school day and it was 421 ms. Figure 4A shows the e.c.g. changes of a healthy 4-yr-old girl undergoing adenoidectomy with Althesin plus halothane anaesthesia. Preanaesthetic QT interval
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TABLE II. Frequency (%) ofc.cg. changes during inhalation anaesthesia with controlled ventilation in different groups. Number of children in parentheses. BBB = bundle branch block. *P<0.05; **P < 0.01 from the corresponding halothane groups
65i
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500
>
UBO >460
(20
I
ii
in
12
(51)
(29)
(16)
(6)
FIG. 2. Preanaesthetic QT intervals in groups anaesthetized with halothane: I = all the children; II = children with no arrhythmias; III = children with junctional rhythm or bundle branch block (BBB); IV = children having BBB with aberrant conduction. Number in parentheses. Bars indicate SEM. * = P < 0 . 0 1 from group II. • - J><0.05 from group III.
FIG. 3. E.c.g. changes of a healthy 9-yr-old boy undergoing T + A under thiopentone and halothane. 1 = Preanaesthetic e.c.g. with QT 594ms. 2 = Dissection of the left tonsil. QT 560 ms. Aberrant conduction with chaotic rhythm. 3 = Twenty seconds later; bifocal ventricular tachycardia. Arrow indicates lignocaine l m g k g ~ ' . Arterial pressure 120/80mmHg. QT 557ms. 4 = Ten seconds after administration of lignocaine; supraventricular regular rhythm with QT 456 ms. 5 = Sinus rhythm after extubation. QT 461 ms. Speed of paper 25mms"'.
was 402 ms. After insertion of the mouth gag there was BBB, which disappeared when the concentration of halothane was reduced. Figure 4B shows the e.c.g. changes in a healthy 5-yr-old girl undergoing adenoidectomy with thiopentone plus halothane anaesthesia. Preanaesthetic QT interval was 465 ms. Pressure on the adenoidectomy bed caused BBB plus aberrant conduction which dis-
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FIG. 1. E e.g. of a healthy 3-yr-old girl undergoing adenoidectomy under thiopentone and enflurane. Typical change in T w4ve during enflurane is seen. 1 = Preanaesthetic e.c.g. with Q1 393 ms. 2 = 3min after enflurane; QT 439 ms and T wave notched. 3 = After adenoidectomy; QT 445 ms and T biphasic 4 - After extubation; QT 432 ms and T wave notched Speed of paper 25mms~ 1 .
CARDIAC ARRHYTHMIA IN CHILDREN
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A.
appeared after cessation of the surgical manipulation. QT interval was significantly longer 45 s after thiopentone (449 + 4 ms) than after venepuncture (430 ± 4 ms); (P< 0.001) (fig. 5) and was further prolonged 30 s after suxamethonium (P<0.02). It remained unchanged 45 s after Althesin compared with after venepuncture. Suxamethonium after Althesin did not prolong QT. In the thiopentone and Althesin groups, the QT intervals during laryngoscopy and intubation remained the same as after suxamethonium. QT interval after inhalation of halothane for 3 min, after tonsillectomy and after extubation did not diffef significantly from the value after intubation (459 ± 8.4 ms), whereas after inhalation of enflurahe for 3 min QT was significantly prolonged (471 ± 4 ms) (P<0.05) and remained so until extubation (fig. 6). QT intervals during enflurane anaesthesia were significantly longer than the corresponding values during halothane anaesthesia. QT interval after inhalation of halothane for 3 min did not differ significantly from the values after intubation in either the thiopentone
(473 ± 15 ms) or the Althesin group (429 ± 7 ms). After inhalation of halothane for 3 min QT was significantly longer in the thiopentone (457 ± 9 ms) compared with the Althesin group (427 ± 5.6 ms) A70I460
-§ 450 |
£ 440 c 430
420
Init.
Vtnep
Int.
FIG. 5. Effect of induction of anaesthesia on QT. Groups comprised 30 to 37 children. Open columns = thiopentone; black columns = Althesin. Bars indicate SEM. Init. = initial value; Venep. = after venepuncture; I.v. an. = 45 s after injection of i.v. anaesthetic; Sux. — 30 s after injection of suxamethonium; Lar. = after laryngoscopy; Int. = after intubation. * = P<0.02; ** = P< 0.001 from the preceding value in the thiopentone group. • = P < 0 . 0 1 ; • • =« P<0.001 from the thiopentone group.
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FIG. 4. A; E.c.g. changes of a healthy 4-yr-old girl undergoing adenoidectomy under Althesin and halothane. 1 = Preanaesthetic e.c.g. with QT 402 ms. 2 = After insertion of the mouth gag. Bundle branch block with QT 438 ms. 3 = Sinus rhythm after extubation. QT 433 ms. B: E.c.g. changes of a healthy 5-yr-old girl undergoing adenoidectomy under thiopentone and halothane. 1 = Preanaesthetic QT 465 ms. 2 = AfteT tamponing the adenoidectomy bed; BBB plus aberrant conduction. QT 473 ms. 3 = After cessation of surgical manipulation; sinus rhythm with QT 461 ms. Speed of paper 25 mm s"'.
658
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•£ <
1 460 C I—
a 420
Lor
Int.
Inh. an, 3 min
After tons.
Ext
500r
Halothane
DISCUSSION
Junctional rhythm occurred in association with both inhalation anaesthetics, but BBB and BBB plus aberrant conduction only with halothane. The preanaesthetic QT interval was significantly prolonged in the children developing BBB plus aberrant conduction. QT was significantly longer after thiopentone plus suxamethonium than after Althesin plus suxamethonium. QT was prolonged significantly during enflurane, but not during halothane anaesthesia.
Junctional rhythm Junctional rhythm occurred in 4-33% in the different anaesthetic groups. These results with halothane are in agreement with those of Alexander (1971), Alexander, Bekheit and Fletcher (1972), Alexander (1974) and Saarnivaara and Kentala (1977), who found junctional rhythm in 33-51% of adults during oral surgery. Halothane has a tendency to cause junctional rhythm (Johnstone, 1956) because it reduces the firing rate of the sino-atrial pacemaker (Flacke and Alper, 1962; Hauswirth and Schaer, 1967; Gersh and Prys-Roberts, 1972). Junctional rhythm occurred during enflurane anaesthesia as often as during halothane anaesthesia. The frequency of junctional rhythm during enflurane anaesthesia in the present study was in the range found by Soderberg and Grattidge (1975) in children. The 420 Inh an. After mechanism by which enflurane causes junctional T mm aden. FIG. 7. (Jhanges in QT during anaesthesia for adenoidec- rhythm cannot be explained. tomy with thiopentone or Althesin. Mean values for 20 to 27 children. Open columns = thiopentone; black columns = Althesin. Bars indicate SEM. Init. = initial value; Lar. = laryngoscopy; Iht. = after intubation; Inh.an. 3 min = after administration of inhalation anaesthetic for 3 min; After aden. = after adenoidectomy; Ext. = after extubation. * = P<0.05; ** = P<0.02; *** = P < 0.001 from the same i.v. anaesthetic in the preceding column. • = P<0.02; • • = P<0.01; • • • = P<0.001 from the thiopentone group.
QRS complex BBB was not seen during enflurane anaesthesia, but occurred in two children anaesthetized with halothane. In six children BBB was associated with aberrant conduction. In addition to junctional rhythm, the other typical e.c.g. changes caused by halothane are ventricular arrhythmia, especially in
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FIG. 6. Changes in QT during anaesthesia for T + A with thiopentone. Mean values for 22 to 25 children. Open columns = halothane; black columns = enflurane. Bars indicate SEM. Init. = Initial value; Lar. = after laryngoscopy; Int. = after intubation; Inh.an.3min = after administration of inhalation anaesthetic for 3 min; After tons. = after tonsillcctomy; Ext. = after extubation. * = P<0.05; ** = P<0.01; *** = P<0.001 from the same inhalation anaesthetic in the preceding column. • = P<0.05; • • = P<0.02; i = P<0.01 from the halothane group.
(P<0.01). QT shortened towards the time of extubation in the thiopentone group and remained the same in the Althesin group. After inhalation of enflurane for 3 min, QT in both the thiopentone and the Althesin groups was significantly longer than the value after intubation and remained so until extubation. After extubation, QT was significantly longer in the thiopentone (478 ± 6.7 ms) compared with the Althesin group (454 + 6.8 ms) (P< 0.02) (fig. 7).
CARDIAC ARRHYTHMIA IN CHILDREN
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the presence of respiratory acidosis, hypoxia or QT interval in association with i.v. anaesthetics and suxamethoniwn other causes of sympathetic stimulation such as Prolongation of QT interval may be congenital nervousness before operation (Apivor, 1960) or surgical manipulation (Alexander, 1971; (Jervell and Lange-Nielsen, 1957; Romano, Alexander, Bekheit and Fletcher, 1972). In the Genme and Pongiglione, 1963; Ward, 1964) or present study, the concentration of oxygen was acquired by administration of quinidine, tricyclic 30% and end-tidal carbon dioxide was 5.5-6%. antidepressants (Schwartz and Wolf, 1978) or Surgical stimulation may be a factor. This is noradrenaline (Abildskov, 1976). Tricyclic antisupported by Alexander (1971) who found that depressants cause accumulation of noradrenaline 23% of his patients developed ectopic rhythms in at extracellular sites (Carlsson et al., 1969). Proresponse to oral surgery under halothane anaes- longation of QT during a hypertensive period has thesia. Alexander, Bekheit and Fletcher (1972) been found in patients with phaeochromocytoma concluded that afferent impulses caused by oral (Cheng and Bashour, 1976). These results give surgery may be mediated by trigeminal nerve further evidence that, in the presence of increased endings and may stimulate nerve centres in the amounts of catecholamines, QT is prolonged. medulla where sympathetic impulses reaching the Hypocalcaemia may prolong QT (Surawicz, 1964). The children in the present study were heart are initiated. healthy and in electrolyte balance. The reason for the occurrence of BBB or BBB QT interval was prolonged significantly after with aberrant conduction during halothane, but not enflurane, anaesthesia may be explained by the thiopentone induction and further after suxamestudy of Atlee and Rusy (1977) who found that thonium given after thiopentone, whereas it enflurane, like halothane (Atlee and Rusy, 1972), remained unchanged after Althesin. Suxameprolongs A-V nodal but not His-Purkinje and thonium given after Althesin did not prolong QT. ventricular conduction. Atlee and Rusy (1977) Thiopentone depresses activity in all excitable suggested that re-entry of excitation requires tissues and increases the plasma concentration of slowing of conduction, unidirectional block and a catecholamines (Goodman and Gilman, 1975). pathway for an entrant impulse to reach the Takki and others (1972) could not find an increase conduction system before arrival of the next in the catecholamines in association with intubanormal impulse from above. This may explain tion after thiopentone plus suxamethonium. In the why, in our study, and in the study of Alexander present study, the reason for prolongation of QT and Murtagh (1979), all the patients who after thiopentone is unexplained. Stimulation of sympathetic ganglia may be caused by suxamedeveloped aberrant conduction also had BBB. Alexander (1971) suggested that the origin of thonium (Gallindo and Davis, 1962; Stoner and aberration is supraventricular because lignocaine Urbach, 1968). Kadis and Gianelly (1973) found was relatively ineffective in abolishing this that thiopentone caused further aberration in arrhythmia. In the present study, however, ligno- patients with Wolf-Parkinson-White syndrome caine abolished aberrant conduction with chaotic and Suppan (1979) has anaesthetized a patient rhythm in three instances. Since the study reported with this disease using Althesin. Ahnve, Lundman here, lignocaine has proved to be ineffective in two and Shoaleh-var (1978) found that the proof 10 children with aberrant conduction during longation of QT was a predictor of ventricular halothane anaesthesia. In the present study, arrhythmia in acute myocardial infarction. aberrant conduction led to bifocal ventricular Althesin may prevent ventricular arrhythmia or tachycardia in a 9-yr-old boy. This arrhythmia aberration by stabilizing the QT interval. might have been fatal without treatment; Gotta and others (1976) have found that aberrant con- QT interval in association with QRS complex duction is a precursor of serious cardiac arrhythchanges mia during halothane anaesthesia for oral surgery. The children with BBB without aberration had a The frequency of BBB plus aberrant conduction normal preanaesthetic QT interval whereas, in after thiopentone induction was twice that after those showing BBB with aberration, QT was Althesin. The antiarrhythmic effect of Althesin significantly prolonged before anaesthesia and was noted by Cundy (1973), Alexander (1974) and during the arrhythmia. One child with a preanaesthetic QT of 594 ms developed bifocal ventricular Saarnivaara and Kentala (1977).
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ACKNOWLEDGEMENTS
I am grateful to L. Saarnivaara, M.D. for discussions and to M. S. Nieminen, M.D. of the Cardiologies] Investigation Department of Helsinki University Hospital for his help in interpreting the electrocardiograms. I wish to thank the nurses specializing in anaesthesia for their unfailing assistance during the course of this study. My thanks are also due to Miss Elizabeth Heap for her help with the English language.
mias in acute myocardial infarction. Ada Med. Scand., 204, 17. Apivor, D. (1960). Halothane. Anaesthesia, 15, 11. Alexander, J. P. (1971). Dysrhythmia and oral surgery. Br. J. Anaesth., 43, 773. (1974). Arrhythmia and oral surgery: induction of anaesthesia with Althesin. Br. J. Anaesth., 46, 770. Bekheit, S., and Fletcher, E. (1972). Dysrhythmia and oral surgery II: junctional rhythms. Br. J. Anaesth., 44, 1179. Murtagh, J. G. (1979). Arrhythmias during oral surgery: fascicular blocks in the cardiac conducting system. Br. J. Anaesth., 51, 149. Atlec, J. L., and Rusy, B. F. (1972). Halothane depression of A-V conduction studied by electrograms of the bundle of His in dogs. Anesthesiology, 36, 112.
(1977). Atrioventricular conduction times and atrioventricular nodal conductivity during enflurane anesthesia in dogs. Anesthesiology, 47, 498. Bazett, H. C. (1920). An analysis of the time relations of the electrocardiograms. Heart, 7, 353. Carlsson, A., Corrodi, H., Fuxe, K., and Hokfelt, T. (1969). Effect of some antidepressant drugs on the depletion of intraneuronal brain catccholamine stores caused by 4,adimethylmetatyramine. Eur. J. Pharmacol., 5, 367. Cheng, T. O., and Bashour, T. T. (1976). Striking electrocardiographic changes associated with pheochromocytoma. Chest, 70, 397. Cundy, J. M. (1973). The antidysrhythmic effect of Althesin. Anaesthesia, 28, 544.
Fisch, C , Oehler, R. C , Miller, J. R., and Redish, C. (1969). Cardiac arrhythmias during oral surgery with halothane-nitrous oxide-oxygen anaesthesia. J.A.M.A., 208, 1829. Flackc, W., and Alper, M. H. (1962). Actions of halothane and norcpinephrine in the isolated mammalian heart. Anesthesiology, 23, 793.
Gallindo, A. H., and Davis, T. B. (1962). Succinylcholine and cardiac excitability. Anesthesiology, 23, 32. Gersh, B. J., and Prys-Roberts, C. (1972). The effects of halothane on the interactions between myocardial contractility, aortic impedance and left ventricular performance. IV: haemodynamic responses to vagus nerve stimulation. Br. J. Anaesth., 44, 1133: Goodman, L. S., and Gilman, A. (1975). The Pharmacological Basis of Therapeutics, 5th edn, p. 106. New York, Toronto and London: Macmillan. Gotta, A. W., Sullivan, C. A., Pelkofski, J., Kangwalklai, S. R., and Kozam, R. (1976). Aberrant conduction as a precursor to cardiac arrhythmias during anaesthesia for oral surgery. J. Oral Surg.,34, 421. Hauswirth, O., and Schaer, H. (1967). Effects of halothane on the sino-atrial node. J. Pharmacol. Exp. Ther., 158, 36. Jervell, A., and Lange-Niclsen, F. (1957). Congenital deafmutism, functional heart disease with prolongation of the QT interval and sudden death. Am. Heart J., 54, 59. Johnstonc, M. (1956). The human cardiovascular response to "Fluothane" anaesthesia. Br. J. Anaesth., 28, 392. Kadis, L. B., and Gianelly, R. E. (1973). Heart and cardiovascular system; in Anesthesia and Uncommon Diseases (eds J.
REFERENCES
Abildskov, J. A. (1976). Adrenergic effects on the QT interval of the electrocardiogram. Am. Heart J., 92, 210. Ahnve, S., Lundman, T., and Shoaleh-var, M. (1978). The relationship between QT interval and ventricular arrhyth-
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tachycardia during halothane anaesthesia. One year later QT was normal. The cause may have been preoperative anxiety. Halothane sensitizes the heart to the arrhythmogenic effect of catecholamines (Raventos, 1956; Katz and Katz, 1966). The prolongation of preanaesthetic QT may reflect high plasma concentrations of catecholamines and has a prognostic value in relation to arrhythmia occurring during oral surgery under halothane anaesthesia. Wig and others (1979) described sudden cardiac arrest during halothane anaesthesia in a patient with a preanaesthetic QT interval of 700 ms. Olley and Fowler (1970) found that propranolol appeared to be effective in patients with congenital prolongation of QT in preventing syncopal ventricular fibrillation. Administration of a betablocker before induction of anaesthesia may be of value in patients with a prolonged preanaesthetic QT interval (Wig et al., 1979). Lignocaine abolished aberrant conduction and normalized the prolonged QT interval. Atlee and Rusy (1977) state that, in addition to slowed conduction and unidirectional block, a potentially re-entrant impulse is required for aberration. The present results indicate that the prolongation of QT interval may activate this impulse. QT interval remained the same, or shortened, during halothane anaesthesia, but was prolonged significantly during the first 3min of enflurane anaesthesia and remained at this value throughout the anaesthesia. In spite of the prolongation of QT, neither aberration nor BBB was seen during enflurane anaesthesia, indicating that enflurane has antiarrhythmic properties. This result is supported by the findings of Reisner and Lippmann (1975) and Williams and Sone (1979), who found significantly fewer ventricular arrhythmias during enflurane than during halothane anaesthesia.
Katz and L. B. Kadis), p. 219. Philadelphia: Saunders. Katz, R. L., and Bigger, J. T. (1970). Cardiac arrhythmias during anesthesia and operation. Anesthesiology, 23, 193. Katz, G. J. (1966). Surgical infiltration of pressor drugs and their interactions with volatile anaesthetics. Br. J.
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CARDIAC ARRHYTHMIA IN CHILDREN
VARIATIONS DE L'ELECTROCARDIOGRAMME PENDANT UNE ANESTHESIE A L'HALOTHANE ET L'ENFLURANE AVANT INTERVENTION CHIRURGICALE SUR DES ENFANTS
4-16% des enfants des groupes a excision des vegetations adenoides et dans 11-33% des cas pour les groupes T + A. Le bloc de branche s'est produit dans 4% des enfants anesthesies a l'halothane, mais aucun cas n'a etc enregistre avec l'enfluranc et il a etc particulierement courant en association avec le thiopentone et les operations de T +A. L'un des patients a souffert d'une tachycardie ventriculaire bifocale. L'intervalle TQ a etc plus long par comparaison avec le temoin apres le thiopentone (P< 0,001) et apres le thiopentone et le suxamcthonium (P<0,02). L'intervalle TQ n'a pas change apres l'Althesine, avec ou sans suxamethonium. L'intervalle TQ moyen avant Panesthesie (± erreur type des moyennes) a ete prolonge d'une maniere significative (492+_ 22 ms; nonnale 440 ms) chez les enfants souffrant d'une conduction anormale avec rythme chaotique, mais il etait normal (438 ± 5ras)lorsque le bloc de branche ou le rythme de jonction ctait present pendant Panesthesie a l'halothane. L'intervalle TQ a etc prolonge d'une maniere significative avec Panesthesie a Penflurane, mais pas avec Panesthesie a l'halothane.
EKG-VERANDERUNGEN BEI KINDERN WAHREND HALOTHAN- UND ENFLURANNARKOSE BEI POLYPEN-UND MANDELRESEKTIONEN ZUSAMMENFASSUNG
EKG-Veranderungen wurden bei 152 Kindern verglichen, die unter Halothan- oder Enflurannarkose einer Adenoidektomie oder Adenotonsillektomie (T + A) ausgesetzt wurden. Synaptischer Rhythmus ergab sich bci 4-16% der AdenoidektomieGruppen und bei 11-33% der T + A-Gruppen. Biindelblockierungen traten bei 4% der mit Halothan narkotisierten Kinder auf, nicht aber bei Enfluran, und war besonders haufig bei Thiopenton und T +A-Operationen; ein Kind entwickelte bifokale Ventrikeltachykardie. Das QT-Intervall war der Kontrolle gegeniiber verlangert bei Thiopenton (P< 0,001) und bei Thiopenton und Suxamethonium (P<0,02). Es blieb unverandert bei Althesin, mit oder ohne Suxamethonium. Das mittlere vornarkotische QT-Intervall (±SEM) war wesentliche verlangert (492 ± 22 ms; normal 440 ms); bei den Kindern, die Leitunregelmassigkeiten mit chaotischem Rhythmus zeigten; es war aber normal (438 ± 5 ms), wenn Btindelblockierungen oder synaptischer Rhythmus wahrend der Halothannarkose zu beobachten war. Das QT-Intcrvall war deutlich verlangert bei Enfluran-, nicht aber bei Halothannarkose.
CAMBIOS EN EL ELECTROENCEFALOGRAMA DE NINOS SOMETIDOS A OPERACIONES QUIRURJICAS DE ADENOIDECTOMIA O DE ADENOTONSILECTOMIA BAJO ANESTESIA CON HALOTANO Y ENFLURANO SUMARIO
RESUME
Se compararon los cambios en el electroencefalograma de 152 On a compare les variations de Pelectrocardiogramme de 152 ninos sometidos a operaciones quirurjicas de adenoidectomia o enfants subissant une excision des vegetations adenoides ou une de adenotonsilectomia (T + A) bajo anestesia con halotano y adeno-amygdalectomie (T + A) sous anesthesie a l'halothane enflurano. El ritmo de union tuvo lugar en un 4-16% de los ou a 1'enflurane. Un rythme de jonction s'est produit dans ninos de los grupos de adenoidectomia y en un 11-33% de los
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Anaesth., 38, 712. Kaufman, L. (1965). Cardiac arrhythmias in dentistry. Lancet, 2,287. Kentala, E., and Repo, U. K. (1979). QT interval prolongation during somatomotor activation as predictor of sudden death after myocardial infarction. Arm. Chn. Res., 11, 42. Olley, F. M., and Fowler, R. S. (1970). The surdocardiac syndrome and therapeutic observations. Br. Heart J., 32, 467. Raventos, J. (1956). The action of "Fluothane"—a new volatile anaesthetic. Br. J. Pharmacol., 11, 394. Reisner, L., and Lippmann, M. (1975). Ventricular arrhythmias after epinephrine injection in enflurane and in halothane anaesthesia. Anesth. Analg. (Cleve.), 54, 468. Romano, C , Genme, G., and Pongiglione, R. (1963). Aritmie cardiache rare dell'ct a pediatrica. II. Ctin. Pedtatr. {Bologna), 45, 656. Saamivaara, L., and Kentala, E. (1977). Comparison of electrocardiographic changes during microlaryngoscopy under halothane anaesthesia induced by Althesin or thiopentone. Acta Anacsthcsiol. Scand., 21, 71. Lauerma, S., and Savolainen, V. P. (1974). Electrocardiographic changes during microlaryngoscopy under halothane anaesthesia. Acta Anaesthesiol. Scand., 18, 249. Schwartz, P. J., Stone, H. L., and Brown, A. M. (1976). Effects of unilateral stellate ganglion blockade on the arrhythmias associated with coronary occlusion. Am. Heart J., 92, 589. Wolf, S. (1978). QT interval prolongation as predictor of sudden death in patients with myocardial infarction. Circulation, 57, 1074. Soderberg, M., and Grattidge, P. (1975). A clinical trial of enflurane in children. Acta Anaesthesiol. Scand., 19, 355. Stoner, T. R., and Urbach, K. F. (1968). Cardiac arrhythmias associated with succinylcholine in a patient with pheochromocytoma. Anesthesiology, 29, 1228. Suppan, P. (1979). Althesin in the Wolf-Parkinson-White syndrome. Br. J. Anaesth., 51, 69. Surawicz, B. (1964). Electrolytes and the electrocardiogram. Mod. Concepts Cardiovasc. Dis., 33, 875. Takki, S., Tammisto, T., Nikki, P., and Jaattela, A. (1972). Effect of laryngoscopy and intubation on plasma catecholamine levels during intravenous induction of anaesthesia. Br. J. Anaesth., 44, 1323. Tuohy, O. (1968). Cardiac arrhythmias during oral surgical procedures. Br. Dent. J., Y2A, 417. Ward, O. C. (1964). New familial cardiac syndrome in children. J. Irish Med. Assoc., 54, 103. Wig, J., Bali, I. M., Singh, R. G., Kataria, R. N., and Khattri, H. N. (1979). Prolonged Q-T interval syndrome. Sudden cardiac arrest during anaesthesia. Anaesthesia, 34, 37. Williams, H. D., and Sone, L. jr (1979). Cardiac arrhythmias during coronary-artery operations with halothane or enflurane anesthesia. Anesthesiology, 50, 551.
662 grupos de T + A. El bloqueo del conjunto de la rama tuvo lugar en un 4% de los nifios anestesiados con halotano, pero no con enflurano, y fue bastante comun en las operaciones de T + A y en lo relativo al uso de tiopentona; uno de los pacientes sufrio taquicardia bifocal del ventriculo. El intervalo QT fue bastante prolongado en comparacion con el grupo de control, dcspues de administrar tiopentona (P< 0,001), y tiopentona y suxametonio (P<0,02). El intervalo QT no cambio despues de la adminis-
BRITISH JOURNAL OF ANAESTHESIA tration de altesin, con o sin suxametonio. El intervalo medio QT preanestesico (±SEM) fue significativamente largo (492±22miliseg.; el normal fue de 440miliseg.) en ninos que mostraban una conduction aberrante con ritmo caotico pero fue normal (438 ± 5 miliseg.) cuando estuvo prcsente el bloqueo del conjunto de la rama o el ritmo de union durante la anestesia con halotano. El intervalo QT se prolongo significativamente con la anestesia de enflurano pero no con la de halotano.
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E.C.G. CHANGES DURING HALOTHANE AND ENFLURANE ANAESTHESIA FOR E.N.T. SURGERY IN CHILDREN L. LlNDGREN SUMMARY
Oral surgery under general anaesthesia may provoke serious cardiac arrhythmia (Kaufman, 1965; Tuohy, 1968), often initiated as a reflex caused by the stimulation of the pharynx and trachea (Katz and Bigger, 1970). Halothane is associated with a high frequency of arrhythmia during oral surgery (Tuohy, 1968; Fisch et al., 1969; Saarnivaara et al., 1974; Gotta et al., 1976). Atlee and Rusy (1972,1977) have shown that halothane prolongs A-V nodal, His-Purkinje and ventricular conduction, whereas enflurane only prolongs A-V nodal conduction in dogs. They concluded that conduction changes such as occur with halothane are necessary for ventricular arrhythmias caused by re-entry of excitation and that enflurane is less likely to cause these arrhythmias. Thiopentone appears to increase aberrant ventricular conduction in patients with Wolf-Parkinson-White syndrome (Kadis and Gianelly, 1973). Cundy (1973) has reported a case in which the administration of Althesin effectively abolished ventricular ectopic beats. Alexander (1974) and Saarnivaara and Kentala (1977) found that Althesin protected against ventricular arrhythmia during oral surgery. Prolongation of the QT interval in e.c.g. is a sign of imbalance in cardiac sympathetic activity LEENA
LINDGREN,
M.D.,
Otolaryngological
Hospital,
University of Helsinki, Haartmaninkatu 4E, SF-00290 Helsinki 29, Finland. 0007-0912/81/060653-10 801.00
(Schwartz, Stone and Brown, 1976). This is associated with ventricular arrhythmia in acute myocardial infarction (Ahnve, Lundman and Shoaleh-var, 1978) and is a predictor of sudden death in this disease (Schwartz and Wolf, 1978). Wig and others (1979) have described sudden cardiac arrest in a patient with a prolonged QT interval during halothane anaesthesia. Kentala and Repo (1979) found a prolonged QT interval during exercise testing to be of prognostic value in relation to survival after acute myocardial infarction. The present study was designed to compare the frequency of cardiac arrhythmia during halothane or enflurane anaesthesia, after induction with thiopentone or Althesin, in children undergoing e.n.t. surgery. The effect of anaesthetics on QT intervals was studied and the changes in QT intervals in association with cardiac arrhythmia were evaluated. PATIENTS AND METHODS
One hundred and fifty-two unselected children, with no cardiac disease, undergoing adenoidectomy or adenotonsillectomy (T + A) were studied (table I). Anaesthesia
Premedication was triclofos 70mgkg~' and atropine 0.03mgkg" 1 given orally about 90min before the start of anaesthesia. A needle was inserted to the left cubital vein. In the adenoidectomy group, 45 children were anaes© Macmillan Publishers Ltd 1981
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E.c.g. changes were compared in 152 children undergoing adenoidectomy or adenotonsillectomy ( T +A) under halothane or enflurane anaesthesia. Junctional rhythm occurred in 4-16% of the children in adenoidectomy groups and in 11-33% in T + A groups. Bundle branch block occurred in 4% of the children anaesthetized with halothane, but not with enflurane and was particularly common in association with thiopentone and T + A operations; one patient had bifocal ventricular tachycardia. QT interval was prolonged compared with control after thiopentone (P<0.001) and thiopentone and suxamethonium (P<0.02). QT interval was not changed after Althesin with or without suxamethonium. Mean preanaesthetic QT interval ( ± SEM) was significantly prolonged (492 ± 22 ms; normal 440 ms) in children showing aberrant conduction with chaotic rhythm, but normal (438 ± 5 ms) when bundle branch block or junctional rhythm was present during halothane anaesthesia. QT interval was prolonged significantly in enflurane but not in halothane anaesthesia.
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TABLE I. Sex, age, weight and haemoglobin concentration in different treatment groups. Mean value +_ SD. Number of children in parentheses
(yr)
Weight (kg)
Haemoglobin (gUtre"')
14 14
4.1 ±2.6 4.7±2.3
17.7±7.6 17.5±4.7
135±7.2 136±9.0
17
7.2±2.8
25.6±9.6
124±8.0
15 14
4.3±2.7 4.9±2.5
18.2±6.5 18.5±5.8
135±9.4 132±7.0
15
6.4±2.7
22.7±8.1
127±8.2
Age
Halothane Adenoidectomy Thiopentone (20) Althesin (25) T +A Thiopentone (27) Enflurane Adenoidectomy Thiopentone (25) Althesin (27) T +A Thiopentone (27)
thetized with halothane (induction with thiopentone 5mgkg~' in 20, Althesin 0.06ml kg"' in 25) and 53 with enflurane (25 and 28). In the T + A group, 27 children were anaesthetized with halothane and 27 with enflurane, in either case following thiopentone 5mgkg"' and suxamethonium l.Smgkg" 1 i.v. The trachea was intubated. Mean delivered concentration of halothane was 1.1 (v/v) and of enflurane 2.0. Both anaesthetics were administered in 70% nitrous oxide in oxygen. A Rees system was used for children weighing less than 25 kg and a circle system with carbon dioxide absorption for the remainder. Ventilation of the lungs was usually controlled, but in a few patients it was assisted. End-tidal carbon dioxide concentration was kept at 5.5-6%. All the children were anaesthetized by the author. The mean duration (+ SD) of anaesthesia for adenoidectomy was 31 +_ 7 min and that of the operation 20+ 7 min. The corresponding figures for T + A were 35 ± 9 min and 24 + 8 min, respectively.
according to the following system. If the P wave preceded the QRS complex and PQ interval was shorter than 0.12 s, the junctional rhythm was considered to be upper junctional. If the P wave was hidden within the QRS complex or if it followed the QRS complex, then the junctional rhythm was considered to be middle or lower junctional, respectively (Saarnivaara and Kentala, 1977). E.cg. changes occurring before the start of inhalation anaesthesia are excluded from this study. QT intervals were measured before the induction of anaesthesia, after laryngoscopy, after intubation, 3 min after the start of the inhalation anaesthesia, after adenoidectomy or T + A and after extubation. From the e.cg. (paper speed 25mms~ 1 ) the QT interval was measured from the onset of QRS complex to the end of the T wave. The mean of four successive beats was determined. Rate correction was made according to the formula: QTC = QT/V(R-R') (Bazett, 1920). QT values exceeding 440 ms were denned as prolonged. To analyse the effects of the induction agents on QT interval, QT intervals were measured Assessment of e.cg. changes and QT interval immediately before and after venepuncture, 45 s Heart rate and the e.cg lead-AVR with three after the i.v. anaesthetic, 30 s after suxamesurface electrodes were displayed continuously on thonium, after laryngoscopy and after intubation. an oscilloscope (Mode 280, Kone Osakeyhtio, Mean age, weight and preanaesthetic QT interval Espoo, Finland) and the e.cg. was recorded. (+ SD) of the children in the thiopentone group Monitoring was started 1 min before the insertion were 5.3 ±0.5 yr, 18.8 + 1.3kg and 432±4 ms and of an i.v. cannula and discontinued 2 min after in the Althesin group 4.6 ± 0.6 yr, 18.5 ± 1.4 kg and extubation. 423 ± 4 ms. The e.cg. recordings were analysed with special Student's t tests for paired and unpaired data reference to bundle branch block and aberrant conduction. Junctional rhythm was classified were used for the statistical analysis of the results.
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Male
CARDIAC ARRHYTHMIA IN CHILDREN RESULTS
The mean preanaesthetic QT intervals ( + SD) ranged from 425 ±39 to 447 +37 ms in different groups. There was no disturbance in the e.c.g. i min before venepuncture. Table II shows that junctional rhythm occurred in 4-16% of the children in the adenoidectomy groups. In the T + A groups, the frequency of junctional rhythm ranged from 11 % to 33%. The frequency of upper and middle junctional rhythms was similar in each group.
655
477 ± 14 ms. In the children treated with lignocaine the mean pretreatment (±SEM) QT interval was 509 +24 ms and decreased significantly after lignocaine, followed by sinus rhythm (437 ± 9.7 ms)(P< 0.05). The T wave became biphasic in 15-41% of the children anaesthetized with enflurane and in 0-8 % anaesthetized with halothane. A typical example of T wave becoming biphasic is shown in figure 1. The arterial pressure was maintained during all types of e.c.g. changes.
QRS complex changes Junctional rhythm
Halothane Adenoidectomy Thiopentone (20) Althesin (25)
Upper
Middle
BBB
BBB + aberrant conduction
Biphasic T-wave
5 16
5 16
0 4
10 4
0 8
30
33
4
11
0
12 4
12 7
0 0
0 0
32** 41**
11
15
0
0
15*
T +A Thiopentone (27) Enflurane Adenoidectomy Thiopentone (25) Althesin (27) T+A Thiopentone (27)
Neither bundle branch block (BBB) nor BBB plus aberrant conduction was seen during enflurane anaesthesia, whereas the frequency of BBB ranged from 0% to 4% and BBB plus aberrant conduction was seen in six children in the halothane groups. Aberrant conduction was always associated with the surgical manipulation. In addition to the results shown in table II, one child in the Althesin plus halothane group developed BBB with aberrant conduction before the start of spontaneous breathing when the endtidal carbon dioxide was 9.5%, but this disappeared after breathing 100% oxygen. In three children BBB and aberrant conduction disappeared without treatment. In the remaining three children, e.c.g. became chaotic and this lasted more than 5 min. Administration of lignocaine lmgkg" 1 i.v. promptly abolished the arrhythmia. The mean duration (+ SEM) of QT interval during BBB with aberrant conduction was
Figure 2 shows that the mean preanaesthetic QT interval was significantly longer (492 ± 22 ms) in the children showing BBB plus aberrant conduction than in the children without e.c.g. changes (426±5.2ms) (P<0.01) and in the children with junctional rhythm or BBB (438 ± 5.3 ms) (P<0.05). Figure 3 shows the e.c.g. changes of a healthy 9-yr-old boy undergoing T + A with halothane anaesthesia. Preanaesthetic QT interval was 594 ms. During the dissection of the left tonsil there wag aberrant conduction with chaotic rhythm which resulted in bifocal ventricular tachycardia. A regular supraventricular rhythm was restored after injection of lignocaine lmgkg" 1 i.v. and sinus rhythm followed. This boy's QT interval was checked 1 year later after a normal school day and it was 421 ms. Figure 4A shows the e.c.g. changes of a healthy 4-yr-old girl undergoing adenoidectomy with Althesin plus halothane anaesthesia. Preanaesthetic QT interval
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TABLE II. Frequency (%) ofc.cg. changes during inhalation anaesthesia with controlled ventilation in different groups. Number of children in parentheses. BBB = bundle branch block. *P<0.05; **P < 0.01 from the corresponding halothane groups
65i
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500
>
UBO >460
(20
I
ii
in
12
(51)
(29)
(16)
(6)
FIG. 2. Preanaesthetic QT intervals in groups anaesthetized with halothane: I = all the children; II = children with no arrhythmias; III = children with junctional rhythm or bundle branch block (BBB); IV = children having BBB with aberrant conduction. Number in parentheses. Bars indicate SEM. * = P < 0 . 0 1 from group II. • - J><0.05 from group III.
FIG. 3. E.c.g. changes of a healthy 9-yr-old boy undergoing T + A under thiopentone and halothane. 1 = Preanaesthetic e.c.g. with QT 594ms. 2 = Dissection of the left tonsil. QT 560 ms. Aberrant conduction with chaotic rhythm. 3 = Twenty seconds later; bifocal ventricular tachycardia. Arrow indicates lignocaine l m g k g ~ ' . Arterial pressure 120/80mmHg. QT 557ms. 4 = Ten seconds after administration of lignocaine; supraventricular regular rhythm with QT 456 ms. 5 = Sinus rhythm after extubation. QT 461 ms. Speed of paper 25mms"'.
was 402 ms. After insertion of the mouth gag there was BBB, which disappeared when the concentration of halothane was reduced. Figure 4B shows the e.c.g. changes in a healthy 5-yr-old girl undergoing adenoidectomy with thiopentone plus halothane anaesthesia. Preanaesthetic QT interval was 465 ms. Pressure on the adenoidectomy bed caused BBB plus aberrant conduction which dis-
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FIG. 1. E e.g. of a healthy 3-yr-old girl undergoing adenoidectomy under thiopentone and enflurane. Typical change in T w4ve during enflurane is seen. 1 = Preanaesthetic e.c.g. with Q1 393 ms. 2 = 3min after enflurane; QT 439 ms and T wave notched. 3 = After adenoidectomy; QT 445 ms and T biphasic 4 - After extubation; QT 432 ms and T wave notched Speed of paper 25mms~ 1 .
CARDIAC ARRHYTHMIA IN CHILDREN
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A.
appeared after cessation of the surgical manipulation. QT interval was significantly longer 45 s after thiopentone (449 + 4 ms) than after venepuncture (430 ± 4 ms); (P< 0.001) (fig. 5) and was further prolonged 30 s after suxamethonium (P<0.02). It remained unchanged 45 s after Althesin compared with after venepuncture. Suxamethonium after Althesin did not prolong QT. In the thiopentone and Althesin groups, the QT intervals during laryngoscopy and intubation remained the same as after suxamethonium. QT interval after inhalation of halothane for 3 min, after tonsillectomy and after extubation did not diffef significantly from the value after intubation (459 ± 8.4 ms), whereas after inhalation of enflurahe for 3 min QT was significantly prolonged (471 ± 4 ms) (P<0.05) and remained so until extubation (fig. 6). QT intervals during enflurane anaesthesia were significantly longer than the corresponding values during halothane anaesthesia. QT interval after inhalation of halothane for 3 min did not differ significantly from the values after intubation in either the thiopentone
(473 ± 15 ms) or the Althesin group (429 ± 7 ms). After inhalation of halothane for 3 min QT was significantly longer in the thiopentone (457 ± 9 ms) compared with the Althesin group (427 ± 5.6 ms) A70I460
-§ 450 |
£ 440 c 430
420
Init.
Vtnep
Int.
FIG. 5. Effect of induction of anaesthesia on QT. Groups comprised 30 to 37 children. Open columns = thiopentone; black columns = Althesin. Bars indicate SEM. Init. = initial value; Venep. = after venepuncture; I.v. an. = 45 s after injection of i.v. anaesthetic; Sux. — 30 s after injection of suxamethonium; Lar. = after laryngoscopy; Int. = after intubation. * = P<0.02; ** = P< 0.001 from the preceding value in the thiopentone group. • = P < 0 . 0 1 ; • • =« P<0.001 from the thiopentone group.
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FIG. 4. A; E.c.g. changes of a healthy 4-yr-old girl undergoing adenoidectomy under Althesin and halothane. 1 = Preanaesthetic e.c.g. with QT 402 ms. 2 = After insertion of the mouth gag. Bundle branch block with QT 438 ms. 3 = Sinus rhythm after extubation. QT 433 ms. B: E.c.g. changes of a healthy 5-yr-old girl undergoing adenoidectomy under thiopentone and halothane. 1 = Preanaesthetic QT 465 ms. 2 = AfteT tamponing the adenoidectomy bed; BBB plus aberrant conduction. QT 473 ms. 3 = After cessation of surgical manipulation; sinus rhythm with QT 461 ms. Speed of paper 25 mm s"'.
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500
•£ <
1 460 C I—
a 420
Lor
Int.
Inh. an, 3 min
After tons.
Ext
500r
Halothane
DISCUSSION
Junctional rhythm occurred in association with both inhalation anaesthetics, but BBB and BBB plus aberrant conduction only with halothane. The preanaesthetic QT interval was significantly prolonged in the children developing BBB plus aberrant conduction. QT was significantly longer after thiopentone plus suxamethonium than after Althesin plus suxamethonium. QT was prolonged significantly during enflurane, but not during halothane anaesthesia.
Junctional rhythm Junctional rhythm occurred in 4-33% in the different anaesthetic groups. These results with halothane are in agreement with those of Alexander (1971), Alexander, Bekheit and Fletcher (1972), Alexander (1974) and Saarnivaara and Kentala (1977), who found junctional rhythm in 33-51% of adults during oral surgery. Halothane has a tendency to cause junctional rhythm (Johnstone, 1956) because it reduces the firing rate of the sino-atrial pacemaker (Flacke and Alper, 1962; Hauswirth and Schaer, 1967; Gersh and Prys-Roberts, 1972). Junctional rhythm occurred during enflurane anaesthesia as often as during halothane anaesthesia. The frequency of junctional rhythm during enflurane anaesthesia in the present study was in the range found by Soderberg and Grattidge (1975) in children. The 420 Inh an. After mechanism by which enflurane causes junctional T mm aden. FIG. 7. (Jhanges in QT during anaesthesia for adenoidec- rhythm cannot be explained. tomy with thiopentone or Althesin. Mean values for 20 to 27 children. Open columns = thiopentone; black columns = Althesin. Bars indicate SEM. Init. = initial value; Lar. = laryngoscopy; Iht. = after intubation; Inh.an. 3 min = after administration of inhalation anaesthetic for 3 min; After aden. = after adenoidectomy; Ext. = after extubation. * = P<0.05; ** = P<0.02; *** = P < 0.001 from the same i.v. anaesthetic in the preceding column. • = P<0.02; • • = P<0.01; • • • = P<0.001 from the thiopentone group.
QRS complex BBB was not seen during enflurane anaesthesia, but occurred in two children anaesthetized with halothane. In six children BBB was associated with aberrant conduction. In addition to junctional rhythm, the other typical e.c.g. changes caused by halothane are ventricular arrhythmia, especially in
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FIG. 6. Changes in QT during anaesthesia for T + A with thiopentone. Mean values for 22 to 25 children. Open columns = halothane; black columns = enflurane. Bars indicate SEM. Init. = Initial value; Lar. = after laryngoscopy; Int. = after intubation; Inh.an.3min = after administration of inhalation anaesthetic for 3 min; After tons. = after tonsillcctomy; Ext. = after extubation. * = P<0.05; ** = P<0.01; *** = P<0.001 from the same inhalation anaesthetic in the preceding column. • = P<0.05; • • = P<0.02; i = P<0.01 from the halothane group.
(P<0.01). QT shortened towards the time of extubation in the thiopentone group and remained the same in the Althesin group. After inhalation of enflurane for 3 min, QT in both the thiopentone and the Althesin groups was significantly longer than the value after intubation and remained so until extubation. After extubation, QT was significantly longer in the thiopentone (478 ± 6.7 ms) compared with the Althesin group (454 + 6.8 ms) (P< 0.02) (fig. 7).
CARDIAC ARRHYTHMIA IN CHILDREN
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the presence of respiratory acidosis, hypoxia or QT interval in association with i.v. anaesthetics and suxamethoniwn other causes of sympathetic stimulation such as Prolongation of QT interval may be congenital nervousness before operation (Apivor, 1960) or surgical manipulation (Alexander, 1971; (Jervell and Lange-Nielsen, 1957; Romano, Alexander, Bekheit and Fletcher, 1972). In the Genme and Pongiglione, 1963; Ward, 1964) or present study, the concentration of oxygen was acquired by administration of quinidine, tricyclic 30% and end-tidal carbon dioxide was 5.5-6%. antidepressants (Schwartz and Wolf, 1978) or Surgical stimulation may be a factor. This is noradrenaline (Abildskov, 1976). Tricyclic antisupported by Alexander (1971) who found that depressants cause accumulation of noradrenaline 23% of his patients developed ectopic rhythms in at extracellular sites (Carlsson et al., 1969). Proresponse to oral surgery under halothane anaes- longation of QT during a hypertensive period has thesia. Alexander, Bekheit and Fletcher (1972) been found in patients with phaeochromocytoma concluded that afferent impulses caused by oral (Cheng and Bashour, 1976). These results give surgery may be mediated by trigeminal nerve further evidence that, in the presence of increased endings and may stimulate nerve centres in the amounts of catecholamines, QT is prolonged. medulla where sympathetic impulses reaching the Hypocalcaemia may prolong QT (Surawicz, 1964). The children in the present study were heart are initiated. healthy and in electrolyte balance. The reason for the occurrence of BBB or BBB QT interval was prolonged significantly after with aberrant conduction during halothane, but not enflurane, anaesthesia may be explained by the thiopentone induction and further after suxamestudy of Atlee and Rusy (1977) who found that thonium given after thiopentone, whereas it enflurane, like halothane (Atlee and Rusy, 1972), remained unchanged after Althesin. Suxameprolongs A-V nodal but not His-Purkinje and thonium given after Althesin did not prolong QT. ventricular conduction. Atlee and Rusy (1977) Thiopentone depresses activity in all excitable suggested that re-entry of excitation requires tissues and increases the plasma concentration of slowing of conduction, unidirectional block and a catecholamines (Goodman and Gilman, 1975). pathway for an entrant impulse to reach the Takki and others (1972) could not find an increase conduction system before arrival of the next in the catecholamines in association with intubanormal impulse from above. This may explain tion after thiopentone plus suxamethonium. In the why, in our study, and in the study of Alexander present study, the reason for prolongation of QT and Murtagh (1979), all the patients who after thiopentone is unexplained. Stimulation of sympathetic ganglia may be caused by suxamedeveloped aberrant conduction also had BBB. Alexander (1971) suggested that the origin of thonium (Gallindo and Davis, 1962; Stoner and aberration is supraventricular because lignocaine Urbach, 1968). Kadis and Gianelly (1973) found was relatively ineffective in abolishing this that thiopentone caused further aberration in arrhythmia. In the present study, however, ligno- patients with Wolf-Parkinson-White syndrome caine abolished aberrant conduction with chaotic and Suppan (1979) has anaesthetized a patient rhythm in three instances. Since the study reported with this disease using Althesin. Ahnve, Lundman here, lignocaine has proved to be ineffective in two and Shoaleh-var (1978) found that the proof 10 children with aberrant conduction during longation of QT was a predictor of ventricular halothane anaesthesia. In the present study, arrhythmia in acute myocardial infarction. aberrant conduction led to bifocal ventricular Althesin may prevent ventricular arrhythmia or tachycardia in a 9-yr-old boy. This arrhythmia aberration by stabilizing the QT interval. might have been fatal without treatment; Gotta and others (1976) have found that aberrant con- QT interval in association with QRS complex duction is a precursor of serious cardiac arrhythchanges mia during halothane anaesthesia for oral surgery. The children with BBB without aberration had a The frequency of BBB plus aberrant conduction normal preanaesthetic QT interval whereas, in after thiopentone induction was twice that after those showing BBB with aberration, QT was Althesin. The antiarrhythmic effect of Althesin significantly prolonged before anaesthesia and was noted by Cundy (1973), Alexander (1974) and during the arrhythmia. One child with a preanaesthetic QT of 594 ms developed bifocal ventricular Saarnivaara and Kentala (1977).
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ACKNOWLEDGEMENTS
I am grateful to L. Saarnivaara, M.D. for discussions and to M. S. Nieminen, M.D. of the Cardiologies] Investigation Department of Helsinki University Hospital for his help in interpreting the electrocardiograms. I wish to thank the nurses specializing in anaesthesia for their unfailing assistance during the course of this study. My thanks are also due to Miss Elizabeth Heap for her help with the English language.
mias in acute myocardial infarction. Ada Med. Scand., 204, 17. Apivor, D. (1960). Halothane. Anaesthesia, 15, 11. Alexander, J. P. (1971). Dysrhythmia and oral surgery. Br. J. Anaesth., 43, 773. (1974). Arrhythmia and oral surgery: induction of anaesthesia with Althesin. Br. J. Anaesth., 46, 770. Bekheit, S., and Fletcher, E. (1972). Dysrhythmia and oral surgery II: junctional rhythms. Br. J. Anaesth., 44, 1179. Murtagh, J. G. (1979). Arrhythmias during oral surgery: fascicular blocks in the cardiac conducting system. Br. J. Anaesth., 51, 149. Atlec, J. L., and Rusy, B. F. (1972). Halothane depression of A-V conduction studied by electrograms of the bundle of His in dogs. Anesthesiology, 36, 112.
(1977). Atrioventricular conduction times and atrioventricular nodal conductivity during enflurane anesthesia in dogs. Anesthesiology, 47, 498. Bazett, H. C. (1920). An analysis of the time relations of the electrocardiograms. Heart, 7, 353. Carlsson, A., Corrodi, H., Fuxe, K., and Hokfelt, T. (1969). Effect of some antidepressant drugs on the depletion of intraneuronal brain catccholamine stores caused by 4,adimethylmetatyramine. Eur. J. Pharmacol., 5, 367. Cheng, T. O., and Bashour, T. T. (1976). Striking electrocardiographic changes associated with pheochromocytoma. Chest, 70, 397. Cundy, J. M. (1973). The antidysrhythmic effect of Althesin. Anaesthesia, 28, 544.
Fisch, C , Oehler, R. C , Miller, J. R., and Redish, C. (1969). Cardiac arrhythmias during oral surgery with halothane-nitrous oxide-oxygen anaesthesia. J.A.M.A., 208, 1829. Flackc, W., and Alper, M. H. (1962). Actions of halothane and norcpinephrine in the isolated mammalian heart. Anesthesiology, 23, 793.
Gallindo, A. H., and Davis, T. B. (1962). Succinylcholine and cardiac excitability. Anesthesiology, 23, 32. Gersh, B. J., and Prys-Roberts, C. (1972). The effects of halothane on the interactions between myocardial contractility, aortic impedance and left ventricular performance. IV: haemodynamic responses to vagus nerve stimulation. Br. J. Anaesth., 44, 1133: Goodman, L. S., and Gilman, A. (1975). The Pharmacological Basis of Therapeutics, 5th edn, p. 106. New York, Toronto and London: Macmillan. Gotta, A. W., Sullivan, C. A., Pelkofski, J., Kangwalklai, S. R., and Kozam, R. (1976). Aberrant conduction as a precursor to cardiac arrhythmias during anaesthesia for oral surgery. J. Oral Surg.,34, 421. Hauswirth, O., and Schaer, H. (1967). Effects of halothane on the sino-atrial node. J. Pharmacol. Exp. Ther., 158, 36. Jervell, A., and Lange-Niclsen, F. (1957). Congenital deafmutism, functional heart disease with prolongation of the QT interval and sudden death. Am. Heart J., 54, 59. Johnstonc, M. (1956). The human cardiovascular response to "Fluothane" anaesthesia. Br. J. Anaesth., 28, 392. Kadis, L. B., and Gianelly, R. E. (1973). Heart and cardiovascular system; in Anesthesia and Uncommon Diseases (eds J.
REFERENCES
Abildskov, J. A. (1976). Adrenergic effects on the QT interval of the electrocardiogram. Am. Heart J., 92, 210. Ahnve, S., Lundman, T., and Shoaleh-var, M. (1978). The relationship between QT interval and ventricular arrhyth-
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tachycardia during halothane anaesthesia. One year later QT was normal. The cause may have been preoperative anxiety. Halothane sensitizes the heart to the arrhythmogenic effect of catecholamines (Raventos, 1956; Katz and Katz, 1966). The prolongation of preanaesthetic QT may reflect high plasma concentrations of catecholamines and has a prognostic value in relation to arrhythmia occurring during oral surgery under halothane anaesthesia. Wig and others (1979) described sudden cardiac arrest during halothane anaesthesia in a patient with a preanaesthetic QT interval of 700 ms. Olley and Fowler (1970) found that propranolol appeared to be effective in patients with congenital prolongation of QT in preventing syncopal ventricular fibrillation. Administration of a betablocker before induction of anaesthesia may be of value in patients with a prolonged preanaesthetic QT interval (Wig et al., 1979). Lignocaine abolished aberrant conduction and normalized the prolonged QT interval. Atlee and Rusy (1977) state that, in addition to slowed conduction and unidirectional block, a potentially re-entrant impulse is required for aberration. The present results indicate that the prolongation of QT interval may activate this impulse. QT interval remained the same, or shortened, during halothane anaesthesia, but was prolonged significantly during the first 3min of enflurane anaesthesia and remained at this value throughout the anaesthesia. In spite of the prolongation of QT, neither aberration nor BBB was seen during enflurane anaesthesia, indicating that enflurane has antiarrhythmic properties. This result is supported by the findings of Reisner and Lippmann (1975) and Williams and Sone (1979), who found significantly fewer ventricular arrhythmias during enflurane than during halothane anaesthesia.
Katz and L. B. Kadis), p. 219. Philadelphia: Saunders. Katz, R. L., and Bigger, J. T. (1970). Cardiac arrhythmias during anesthesia and operation. Anesthesiology, 23, 193. Katz, G. J. (1966). Surgical infiltration of pressor drugs and their interactions with volatile anaesthetics. Br. J.
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CARDIAC ARRHYTHMIA IN CHILDREN
VARIATIONS DE L'ELECTROCARDIOGRAMME PENDANT UNE ANESTHESIE A L'HALOTHANE ET L'ENFLURANE AVANT INTERVENTION CHIRURGICALE SUR DES ENFANTS
4-16% des enfants des groupes a excision des vegetations adenoides et dans 11-33% des cas pour les groupes T + A. Le bloc de branche s'est produit dans 4% des enfants anesthesies a l'halothane, mais aucun cas n'a etc enregistre avec l'enfluranc et il a etc particulierement courant en association avec le thiopentone et les operations de T +A. L'un des patients a souffert d'une tachycardie ventriculaire bifocale. L'intervalle TQ a etc plus long par comparaison avec le temoin apres le thiopentone (P< 0,001) et apres le thiopentone et le suxamcthonium (P<0,02). L'intervalle TQ n'a pas change apres l'Althesine, avec ou sans suxamethonium. L'intervalle TQ moyen avant Panesthesie (± erreur type des moyennes) a ete prolonge d'une maniere significative (492+_ 22 ms; nonnale 440 ms) chez les enfants souffrant d'une conduction anormale avec rythme chaotique, mais il etait normal (438 ± 5ras)lorsque le bloc de branche ou le rythme de jonction ctait present pendant Panesthesie a l'halothane. L'intervalle TQ a etc prolonge d'une maniere significative avec Panesthesie a Penflurane, mais pas avec Panesthesie a l'halothane.
EKG-VERANDERUNGEN BEI KINDERN WAHREND HALOTHAN- UND ENFLURANNARKOSE BEI POLYPEN-UND MANDELRESEKTIONEN ZUSAMMENFASSUNG
EKG-Veranderungen wurden bei 152 Kindern verglichen, die unter Halothan- oder Enflurannarkose einer Adenoidektomie oder Adenotonsillektomie (T + A) ausgesetzt wurden. Synaptischer Rhythmus ergab sich bci 4-16% der AdenoidektomieGruppen und bei 11-33% der T + A-Gruppen. Biindelblockierungen traten bei 4% der mit Halothan narkotisierten Kinder auf, nicht aber bei Enfluran, und war besonders haufig bei Thiopenton und T +A-Operationen; ein Kind entwickelte bifokale Ventrikeltachykardie. Das QT-Intervall war der Kontrolle gegeniiber verlangert bei Thiopenton (P< 0,001) und bei Thiopenton und Suxamethonium (P<0,02). Es blieb unverandert bei Althesin, mit oder ohne Suxamethonium. Das mittlere vornarkotische QT-Intervall (±SEM) war wesentliche verlangert (492 ± 22 ms; normal 440 ms); bei den Kindern, die Leitunregelmassigkeiten mit chaotischem Rhythmus zeigten; es war aber normal (438 ± 5 ms), wenn Btindelblockierungen oder synaptischer Rhythmus wahrend der Halothannarkose zu beobachten war. Das QT-Intcrvall war deutlich verlangert bei Enfluran-, nicht aber bei Halothannarkose.
CAMBIOS EN EL ELECTROENCEFALOGRAMA DE NINOS SOMETIDOS A OPERACIONES QUIRURJICAS DE ADENOIDECTOMIA O DE ADENOTONSILECTOMIA BAJO ANESTESIA CON HALOTANO Y ENFLURANO SUMARIO
RESUME
Se compararon los cambios en el electroencefalograma de 152 On a compare les variations de Pelectrocardiogramme de 152 ninos sometidos a operaciones quirurjicas de adenoidectomia o enfants subissant une excision des vegetations adenoides ou une de adenotonsilectomia (T + A) bajo anestesia con halotano y adeno-amygdalectomie (T + A) sous anesthesie a l'halothane enflurano. El ritmo de union tuvo lugar en un 4-16% de los ou a 1'enflurane. Un rythme de jonction s'est produit dans ninos de los grupos de adenoidectomia y en un 11-33% de los
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Anaesth., 38, 712. Kaufman, L. (1965). Cardiac arrhythmias in dentistry. Lancet, 2,287. Kentala, E., and Repo, U. K. (1979). QT interval prolongation during somatomotor activation as predictor of sudden death after myocardial infarction. Arm. Chn. Res., 11, 42. Olley, F. M., and Fowler, R. S. (1970). The surdocardiac syndrome and therapeutic observations. Br. Heart J., 32, 467. Raventos, J. (1956). The action of "Fluothane"—a new volatile anaesthetic. Br. J. Pharmacol., 11, 394. Reisner, L., and Lippmann, M. (1975). Ventricular arrhythmias after epinephrine injection in enflurane and in halothane anaesthesia. Anesth. Analg. (Cleve.), 54, 468. Romano, C , Genme, G., and Pongiglione, R. (1963). Aritmie cardiache rare dell'ct a pediatrica. II. Ctin. Pedtatr. {Bologna), 45, 656. Saamivaara, L., and Kentala, E. (1977). Comparison of electrocardiographic changes during microlaryngoscopy under halothane anaesthesia induced by Althesin or thiopentone. Acta Anacsthcsiol. Scand., 21, 71. Lauerma, S., and Savolainen, V. P. (1974). Electrocardiographic changes during microlaryngoscopy under halothane anaesthesia. Acta Anaesthesiol. Scand., 18, 249. Schwartz, P. J., Stone, H. L., and Brown, A. M. (1976). Effects of unilateral stellate ganglion blockade on the arrhythmias associated with coronary occlusion. Am. Heart J., 92, 589. Wolf, S. (1978). QT interval prolongation as predictor of sudden death in patients with myocardial infarction. Circulation, 57, 1074. Soderberg, M., and Grattidge, P. (1975). A clinical trial of enflurane in children. Acta Anaesthesiol. Scand., 19, 355. Stoner, T. R., and Urbach, K. F. (1968). Cardiac arrhythmias associated with succinylcholine in a patient with pheochromocytoma. Anesthesiology, 29, 1228. Suppan, P. (1979). Althesin in the Wolf-Parkinson-White syndrome. Br. J. Anaesth., 51, 69. Surawicz, B. (1964). Electrolytes and the electrocardiogram. Mod. Concepts Cardiovasc. Dis., 33, 875. Takki, S., Tammisto, T., Nikki, P., and Jaattela, A. (1972). Effect of laryngoscopy and intubation on plasma catecholamine levels during intravenous induction of anaesthesia. Br. J. Anaesth., 44, 1323. Tuohy, O. (1968). Cardiac arrhythmias during oral surgical procedures. Br. Dent. J., Y2A, 417. Ward, O. C. (1964). New familial cardiac syndrome in children. J. Irish Med. Assoc., 54, 103. Wig, J., Bali, I. M., Singh, R. G., Kataria, R. N., and Khattri, H. N. (1979). Prolonged Q-T interval syndrome. Sudden cardiac arrest during anaesthesia. Anaesthesia, 34, 37. Williams, H. D., and Sone, L. jr (1979). Cardiac arrhythmias during coronary-artery operations with halothane or enflurane anesthesia. Anesthesiology, 50, 551.
662 grupos de T + A. El bloqueo del conjunto de la rama tuvo lugar en un 4% de los nifios anestesiados con halotano, pero no con enflurano, y fue bastante comun en las operaciones de T + A y en lo relativo al uso de tiopentona; uno de los pacientes sufrio taquicardia bifocal del ventriculo. El intervalo QT fue bastante prolongado en comparacion con el grupo de control, dcspues de administrar tiopentona (P< 0,001), y tiopentona y suxametonio (P<0,02). El intervalo QT no cambio despues de la adminis-
BRITISH JOURNAL OF ANAESTHESIA tration de altesin, con o sin suxametonio. El intervalo medio QT preanestesico (±SEM) fue significativamente largo (492±22miliseg.; el normal fue de 440miliseg.) en ninos que mostraban una conduction aberrante con ritmo caotico pero fue normal (438 ± 5 miliseg.) cuando estuvo prcsente el bloqueo del conjunto de la rama o el ritmo de union durante la anestesia con halotano. El intervalo QT se prolongo significativamente con la anestesia de enflurano pero no con la de halotano.
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