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GENERAL ANAESTHESIA IN COMPLETE HEART BLOCK
Brit. J. Anaesth. (1962), 34, 102
GENERAL ANAESTHESIA IN COMPLETE HEART BLOCK BY
EDWARD D. T. ROSS
Department of Anaesthetics, Glasgow Royal Infirmary, Scotland
CASE REPORT The patient, a frail man aged 80 years, was admitted to the Burns Unit of Glasgow Roval Infirmary on
March 4, 1960, having been severely burned on the lower extremities five days previously. He was debilitated, suffering from severe chronic bronchitis and had a pulse rate of 38 beats per minute, strongly suggestive of complete heart block. His burning injuries were presumed to have been sustained during a Stokes-Adams attack. The e.c.g. (fig. 1) showed complete heart block with an intraventricular conduction defect and right bundle branch block. There was also evidence of widespread myocardial ischaemia. It was difficult to tell whether there had been a recent coronary artery thrombosis or not. He was mildly confused, incontinent of urine and had pressure sores in the lumbosacral region. Anaesthetic management. In view of his incontinence and the pressure sores, spinal and extradural techniques were not considered. He was premedicated with atropine 0.9 mg subcutaneously. After pre-oxygenation, anaesthesia was induced with nitrous oxide, oxygen and ether. The induction was stormy and a few breaths of trichloroethylene were given in the hope of obtunding laryngeal reflexes, but without success. In order to avoid any further hypoxia suxamethonium 60 mg was given intravenously and the patient was intubated. Anaesthesia was continued with nitrous oxide, oxygen and minimal ether, respiration being assisted until the patient's own efforts were considered
FIG. 1 This figure shows a part of the record of lead V2 of the e.c.g. and demonstrates complete heart block with a right bundle branch block. 102
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Modern anaesthesia has made surgery feasible in almost all patients. The anaesthetist is therefore faced from time to time with gravely ill patients requiring operative treatment. Recently an elderly man with complete heart block who had sustained severe burning injuries during a StokesAdams attack was presented for desloughing and skin grafting. Faced with this problem, reference was made to the current British textbooks, but they made scant reference to the particular problems of anaesthesia in complete heart block. As sympathomimetic amines are commonly used in the treatment of complete heart block in an attempt to maintain the idioventricular rate, it was decided to use an anaesthetic known to be a potent sympathetic stimulant, namely diethyl ether. In addition light ether causes minimal circulatory depression.
GENERAL ANAESTHESIA EN COMPLETE HEART BLOCK
COMMENT
The anaesthetic technique chosen was not wholly satisfactory. Two episodes of cardiac arrest occurred during anaesthesia. The first may have been precipitated by mild hypoxia caused through the patient coughing on his endotracheal tube, the second appeared to be quite spontaneous. Hyperventilation, an indirect method of cardiac massage (Bencini and Parola, 1956), restarted the heart on the first occasion. This suggested asystole rather fhan ventricular fibrillation and it was therefore felt that intracardiac adrenaline was a justifiable procedure when the heart failed to restart on the second occasion. This case with its attendant difficulties stimulated interest in the problem of anaesthesia in patients with complete heart block. Current textbooks were of little help, and a search of the literature on the subject was undertaken. MECHANISM, PATHOLOGY AND PROGNOSIS IN COMPLETE HEART BLOCK
In the normal heart the cardiac impulse is initiated in the sino-auricular node or pacemaker, which is specialized cardiac tissue situated near the entry of the superior vena cava into the right auricle. It spreads through the auricular muscle to the
auriculo-ventricular node at the base of the inter-auricular septum and thence via the bundle of His in the interventricular septum. It then divides into right and left bundles to supply each ventricle. In complete heart block the continuity of the bundle of His is interrupted and impulses originating from a source above cannot be relayed to the ventricles. Nevertheless the ventricles are still capable of initiating a beat below the block and this intrinsic or idioventricular rate is slower than that from the normal pacemaker, being about 35 beats per minute. It should be observed that the vagus exerts no direct influence on the ventricle. Its action is on the pacemaker and auriculo-ventricular node, and from these sites vagal action is mediated through the bundle of His to the ventricles. The sympathetic nerves on the other hand act directly on the ventricles, as well as through the bundle of His (Best and Taylor, 1952). It follows, therefore, that in complete heart block the ventricles may be free of vagal influence, while the sympathetic nervous system will still exert considerable control. Rowe and White (1958) studied 278 cases of complete heart block. They considered that coronary artery disease with or without hypertension or acute infarction was responsible for 70 per cent of these. The remainder occurred in patients with rheumatic heart disease, congenital heart disease, digitalis poisoning and other less common cardiac ailments. Except in the congenital and digitalis-induced varieties the condition was twice as common in males. In the coronary group the mean survival time was 4 years. StokesAdams attacks occurred in 38 per cent of the group and, rather surprisingly, these cases had the better prognosis. In the congenital group the prognosis is good and symptoms due to heart block are relatively uncommon. STOKES-ADAMS ATTACKS UNDER ANAESTHESIA
Stokes-Adams attacks occurring under anaesthesia have been described by McLemore and Levine (1955), Hodges et al. (1957), Vandam and McLemore (1957) and Zoll (1958). The series reported by Vandam and McLemore of 22 cases of complete heart block included 11 who had suffered Stokes-Adams attacks preoperatively. Of these 11 cases, 5 had Stokes-
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adequate. After 10 minutes the patient began to gag on the endotracheal tube and an attempt was made to increase the ether concentration. The pulse had been continuously monitored and up until this time had been regular and of good quality although still only 38 beats per minute. It now became impalpable and the patient became apnoeic. Absence of the heartbeat was confirmed by auscultation of the praecordium. Anaesthesia was discontinued, hyperventilation with pure oxygen instituted and the head of the table lowered. Thirty seconds later the radial pulse was again palpable, of good volume and regular at 36 beats per minute. Spontaneous respiration recommenced and a mixture of nitrous oxide with oxygen 30 per cent was sufficient to maintain a satisfactory level of anaesthesia. Desloughing was quickly performed but, just after the skin grafts had been cut, cardiac arrest again occurred, heart sounds again being inaudible. The previous regime was again adopted but this time without success. After 80 seconds 3 ml of 1/10.000 adrenaline, previously prepared against such an emergency, was injected into the left ventricle. The heart restarted immediately at a rate of 96 beats per minute and the operation was rapidly concluded. Ephedrine 30 mg was injected intramuscularly and the patient returned to the ward where oxygen was given. He recovered consciousness in 20 minutes and there were no demonstrable sequelae. The pulse reverted to its former rate of 38 per minute.
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PRE-OPERATIVE DRUG THERAPY
Digitalis. If cardiac failure is present the use of digitalis is indicated to treat this condition. Conversely if digitalis is responsible for the heart block, withdrawal of the drug will reverse the condition. Atropine. Zoll (1958) recommends the use of atropine 1 mg intravenously as a pre-operative screening test to assess the role, if any, which the vagus may have in the production of the block. If a beneficial result is obtained the use of atropine in a dosage of 1 mg 4-hourly during anaesthesia should be considered. Sympathomimetic drugs. Ephedrine orally or isoprenaline sublingually should be administered to stimulate the idioventricukr centre and abolish the Stokes-Adams attacks if possible. These drugs should be administered in increasing dosage until the desired effect is obtained or toxic symptoms like cerebral irritability, spasm of sphincters, excessive hypertension, or ventricular irritability develop (Zoll, 1958). SUGGESTED ANAESTHETIC MANAGEMENT OF PATIENTS WITH
ESTABLISHED
COMPLETE HEART
BLOCK
Premedication. Vandam and McLemore (1957) suggest that opiates and pethidine cause both central and peripheral circulatory depression and recommend the use of a small dose of a barbiturate. It is, however, probably better to avoid all sedative agents in premedicating these patients. Atropine should be given in therapeutic dosage for its
antisialogogue effect but the administration of large doses, in an attempt to speed up the heart rate, may block the sympathetic ganglia and interfere with sympathetic influences on the ventricular pacemaker (Vandam and McLemore, 1957). Kayden and Stack (1955) have shown that intravenous atropine in complete heart block causes atrial tachycardia but rarely influences the ventricular rate. Nevertheless in cases which on pre-operative testing have shown a beneficial effect to the atropine this should probably be given 4-hourly as suggested by Zoll (1958). Anaesthetic agents. Although ether appears to have been the main anaesthetic agent used, Vandam and McLemore (1957) suggest that the agents are not as important as the skill with which they are used. While this may be so, it is felt that in the possible absence of vagal influence on the ventricle, the use of agents such as cyclopropane, trichloroethylene, chloroform and halothane, which are known to be potentially dangerous in the presence of adrenaline (Wylie and Churchill-Davidson, 1960), may well be equally hazardour i : a situation where the sympathetic nerves alone influence the ventricle. Further proof of this theory is given in a report by Cowan (1954). Here cyclopropane caused ventricular extrasystoles, proceeding to multifocal ventricular tachycardia of 90 per minute, when introduced into an anaesthetic for herniorrhaphy in a patient with complete heart block (anaesthesia had been induced with thiopentone and d-tubocurarine had been used). These undesirable effects disappeared in the reverse order on withdrawing the cyclopropane. A further contraindication to the above agents lies in the fact that if asystole occurs while they are being used, the use of intracardiac adrenaline as a resuscitative measure might precipitate ventricular fibrillation and this would necessitate emergency thoracotomy with its attendant hazards. Complete heart block is usually associated with a marked decrease in cardiac output. Despite an increased stroke volume, the heart cannot increase its rate sufficiently to compensate for this decrease in output (Cecil and Loeb, 1959). The dangers of using thiopentone in these circumstances are well known to all anaesthetists and many will feel it is wise to avoid the use of this
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Adams attacks during anaesthesia. Of the 11 not suffering Stokes-Adams attacks pre-operatively only 1 had a cardiac arrest preceded by convulsions which occurred during a caudal block and this could have been a toxic reaction to the local anaesthetic. Four of the episodes of cardiac arrest took place before surgery commenced and on two occasions the arrest was associated with endotracheal intubation. The authors suggest as a possible causative mechanism in the latter two cases, laryngeal reflexes, which might not be vagal in origin, quoting King et al. (1951). Thoracotomy was carried out on only one occasion and this could probably have been avoided
GENERAL ANAESTHESIA IN COMPLETE HEART BLOCK drug. If, however, it is used it should be given in dilute solution, slowly and in minimal dosage.
Drug therapy during operation. Should the heart show signs of excessive slowing during the operative procedure, the use of an isoprenaline or adrenaline drip should be considered. Zoll et al. (1958) compared the effects of these two drugs when given by intravenous infusion to twenty-one patients with complete heart block and found that they both have a beneficial effect on the idioventricular pacemaker. Adrenaline tended to cause the blood pressure to rise, while isoprenaline had the opposite effect and they suggested that the level of the blood pressure should determine which one is used. Isoprenaline was infused at a rate of 5 to 43 ^g per minute (mean 12 ^g per minute) and adrenaline at 5 to 44 (Ag per minute (mean 20 jig per minute). Both drugs were given in 1/250,000 solution at an infusion rate of 1 ml/min (approximately 15 drops per minute) and the patient received 4 ^g per minute. The rate of infusion was regulated in accordance with the e.c.g. tracing. They regarded a rise in the idioventricular rate to over 50 beats per minute or premature ventricular beats at an interval of less than 1.2 seconds as potentially toxic manifesta-
tions. Multifocal ventricular rhythm below 50 per minute was ignored as they pointed out that it can occur spontaneously in complete heart block. Drugs such as quinidine and procaine amide should never be given in an attempt to correct any ventricular arrhythmias which may develop during the course of anaesthesia. Paradoxically if ventricular irritability is present, but the basic rhythm is slow, Zoll (1958) recommends the cautious infusion of a sympathomimetic amine in an attempt to accelerate the idioventricular rhythm and thereby abolish the multifocal ventricular irritability. Mechanical means of treatment. Should drug therapy, cither intravenous or intracardiac, be unsuccessful an artificial pacemaker, which can be introduced percutaneously as described by Ross and Harkins (1959), should be available. Briefly this consists of the percutaneous introduction of an active electrode through the chest into the ventricle by means of a No. 16 hollow needle. The needle is first withdrawn and then the electrode is withdrawn until it passes from the cavity of the ventricle into the ventricular muscle mass. The heart should now start to contract at the rate to which the pacemaker has been set. An indifferent electrode is attached to the epigastrium. There is a slight risk of explosion with this apparatus if ether has been in use. It is advisable to have the patient's expirations conducted out of theatre by means of the T-piece described by Bullough in 1954. The latter could at least be available if not actually used during the anaesthetic procedure. If the patient fails to respond to the above regime or ventricular fibrillation ensues, external cardiac massage should be immediately begun (Kouwenhoven, Jude and Knickerbocker, 1960) while preparations are made speedily for thoracotomy with direct cardiac massage and possible electrical defibrillation. SUMMARY
The anaesthetic management of a case of complete heart block with associated Stokes-Adams attacks is described. During nitrous oxide, oxygen and ether anaesthesia administered via an endotracheal tube, two episodes of cardiac arrest occurred. The first was probably associated with
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Muscle relaxants. Gallamine is considered to be the relaxant of choice. The tachycardia which it usually causes is considered undesirable in patients with cardiac disease but this is unlikely to occur in patients with complete heart block as it is due to a vagolytic action identical to that caused by atropine (Riker and Wescoe, 1951). This has already been shown to be unlikely to influence the ventricular rate. The potentiating effect of ether on the myoneural blockade produced by gallamine must be borne in mind. The occasional tendency of d-tubocurarine to cause hypotension (Thomas, 1957) is considered to limit its value in patients with complete heart Mock. Although bradycardia, cardiac arrhythmias ^i i tran 'e:ic cardiac arrest have been reported fo:>".ing intermittent suxamethonium (Bullougli , ^ 5 r : Lupprian and Churchill-Davidson, 19*"'. ?. sLn^c injection of the drug may probably n. j . ~u .* "sly to facilitate endotracheal intubation when tne patient is thereafter being allowed to breathe spontaneously.
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ACKNOWLEDGMENTS
I wish to thank Mr. J. Scott Tough, Regional Consultant in Plastic and Maxillo-Facial Surgery, for
permission to publish the case report; also Dr. J. H. Wright Consultant Physician, Glasgow Royal Infirmary, for permission to reproduce the e.c.g. I would also like to thank Dr. Walter Norris for helpful advice during the preparation of this paper and Miss Janet Chalmers for secretarial help.
REFERENCES
Bencini, A., and Parola, P. L. (1956). "Pneumomassage" of the heart. Surgery, 39, 375. Best, C H., and Taylor, N. B. (1952). The Living Body, 3rd ed., pp. 203, 204. London: Chapman and Hall. Bullough, J. (1954). Anaesthetic explosions: prevention by withdrawal methods. Lancet, 1, 798. (1959). Intermittent suxamethonium injections. Brit. med. J.. 1, 786. Cecil, R. L., and Loeb, R. F. (1959). A Textbook of Medicine, 10th ed., p. 1311. Philadelphia and London: Saunders. Cowan, K. A. (1954). Heart block and cyclopropane. Anaesthesia, 54, 114. Hodges, R. J. H., Witzeman, R. A., and Leigh, M. A. (1957). Multiple Stokes-Adams episodes during anaesthesia. Brit. med. J., 1, 625. Kayden, H. J., and Stack, M. (1955). Studies on complete atrio-ventricular dissociation with special reference to Stokes-Adams syndrome. Abstracted Circulation, 12, 729. King, B. D., Harris, L. C , Greifenstein, F. E., Elder, J. D., and Dripps, R. D. (1951). Reflex circulatory responses to direct laryngoscopy and tracheal intubation performed during general anesthesia. Anesthesiology, 12, 556. Kouwenhoven, W. B., Jude, J. R., and Knickerbocker, G. G. (1960). Closed-chest cardiac massage; /. Amer. med. Ass., 173, 1064. Lupprian, K. G., and Churchill-Davidson, H. C (1960). Effects of suxamethonium on cardiac rhythm. Brit. med. J., 2, 1774. McLemore, G. A., and Levine, S. A. (1955). Possible therapeutic value of cholecystectomy in AdamsStokes disease. Amer. J. med. Sci., 229, 386. Riker, W. F., and Wescoe, W. C. (1951). The pharmacology of Flaxedil with observations on certain analogs. Ann. N.Y. Acad. Sci., 54, 373. Ross, J. K., and Harkins, G. A. (1959). Percutaneous introduction of cardiac pacemaker electrode. Lancet, 2, 1109. Rowe, J. C , and White, P. D. (1958). Complete heart block: a follow-up study. Ann. intern. Med., 49, 260. Thomas, E. T. (1957). The effects of d-tubocurarine on the blood pressure of anaesthetized patients. Lancet, 2, 772. Vandam, L. D., and McLemore, G. A. (1957). Circulatory arrest in patients with complete heart block during anesthesia and surgery. Ann. intern. Med., 47, 518. Wylie, W. D., and Churchill-Davidson, H. G. (1960). A Practice of Anaesthesia, p. 673. London: Lloyd-Luke. Zoll, P. M. U958). Anesthesia in patients with atrioventricular block. Curr. Res. Anesth. Analg., 37, 148. Linenthal, A. J., Gibson, W., Paul. M. H., and Norman, L. R. (1958). Intravenous therapy of Stokes-Adams disease. Circulation, 17, 325.
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mild hypoxia, but there was no obvious reason for the second. The heart was restarted by pneumomassage (hyperventilation of the lungs with oxygen) on the first occasion and by the administration of intracardiac adrenaline on the second. After a search of the literature certain recommendations are made. Atropine 1 mg intravenously is a useful preoperative test to detect the occasional case of complete heart block due to vagal overactivity. Cases which show benefit should be given atropine 1 mg 4-hourly to cover anaesthesia. The pre-operative administration of ephedrine or isoprenaline is recommended until benefit is obtained or toxic reactions to these drugs appear. Digitalis should be used if cardiac failure is present. Some cases of complete heart block are due to digitalis overdose and withdrawal of the drug will cure the condition. In pre-anaesthetic medication depressant drugs like morphine and the barbiturates are best avoided. Atropine should be used as an antisialogogue in appropriate dosage but the use of large doses in an attempt to speed up the ventricular rate may be dangerous. Continuous electrocardiography is mandatory during anaesthesia. Reasons are given for the avoidance of thiopentone, cyclopropane and halogenated hydrocarbons. Minimal ether has certain desirable features, such as its sympathomimetic effects and lack of serialization of the myocardium. A single dose of suxamethonium would appear reasonable to facilitate intubation and gallamine is recommended as the relaxant of choice for intraabdominal procedures or when controlled respiration is indicated. A 1/250,000 solution of adrenaline or isoprenaline should be available to counteract excessive slowing of the heart, the former being preferred if there is associated hypotension and the latter if there is associated hypertension. The cautious infusion of a sympathomimetic amine may abolish multifocal ventricular irritability at slow rates by speeding up the idioventricular rhythm. The use of procaine amide and quinidine should be avoided. The use of percutaneous cardiac pacemaker and closed cardiac massage is discussed.
GENERAL ANAESTHESIA IN COMPLETE HEART BLOCK BY
EDWARD D. T. ROSS
Department of Anaesthetics, Glasgow Royal Infirmary, Scotland
CASE REPORT The patient, a frail man aged 80 years, was admitted to the Burns Unit of Glasgow Roval Infirmary on
March 4, 1960, having been severely burned on the lower extremities five days previously. He was debilitated, suffering from severe chronic bronchitis and had a pulse rate of 38 beats per minute, strongly suggestive of complete heart block. His burning injuries were presumed to have been sustained during a Stokes-Adams attack. The e.c.g. (fig. 1) showed complete heart block with an intraventricular conduction defect and right bundle branch block. There was also evidence of widespread myocardial ischaemia. It was difficult to tell whether there had been a recent coronary artery thrombosis or not. He was mildly confused, incontinent of urine and had pressure sores in the lumbosacral region. Anaesthetic management. In view of his incontinence and the pressure sores, spinal and extradural techniques were not considered. He was premedicated with atropine 0.9 mg subcutaneously. After pre-oxygenation, anaesthesia was induced with nitrous oxide, oxygen and ether. The induction was stormy and a few breaths of trichloroethylene were given in the hope of obtunding laryngeal reflexes, but without success. In order to avoid any further hypoxia suxamethonium 60 mg was given intravenously and the patient was intubated. Anaesthesia was continued with nitrous oxide, oxygen and minimal ether, respiration being assisted until the patient's own efforts were considered
FIG. 1 This figure shows a part of the record of lead V2 of the e.c.g. and demonstrates complete heart block with a right bundle branch block. 102
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Modern anaesthesia has made surgery feasible in almost all patients. The anaesthetist is therefore faced from time to time with gravely ill patients requiring operative treatment. Recently an elderly man with complete heart block who had sustained severe burning injuries during a StokesAdams attack was presented for desloughing and skin grafting. Faced with this problem, reference was made to the current British textbooks, but they made scant reference to the particular problems of anaesthesia in complete heart block. As sympathomimetic amines are commonly used in the treatment of complete heart block in an attempt to maintain the idioventricular rate, it was decided to use an anaesthetic known to be a potent sympathetic stimulant, namely diethyl ether. In addition light ether causes minimal circulatory depression.
GENERAL ANAESTHESIA EN COMPLETE HEART BLOCK
COMMENT
The anaesthetic technique chosen was not wholly satisfactory. Two episodes of cardiac arrest occurred during anaesthesia. The first may have been precipitated by mild hypoxia caused through the patient coughing on his endotracheal tube, the second appeared to be quite spontaneous. Hyperventilation, an indirect method of cardiac massage (Bencini and Parola, 1956), restarted the heart on the first occasion. This suggested asystole rather fhan ventricular fibrillation and it was therefore felt that intracardiac adrenaline was a justifiable procedure when the heart failed to restart on the second occasion. This case with its attendant difficulties stimulated interest in the problem of anaesthesia in patients with complete heart block. Current textbooks were of little help, and a search of the literature on the subject was undertaken. MECHANISM, PATHOLOGY AND PROGNOSIS IN COMPLETE HEART BLOCK
In the normal heart the cardiac impulse is initiated in the sino-auricular node or pacemaker, which is specialized cardiac tissue situated near the entry of the superior vena cava into the right auricle. It spreads through the auricular muscle to the
auriculo-ventricular node at the base of the inter-auricular septum and thence via the bundle of His in the interventricular septum. It then divides into right and left bundles to supply each ventricle. In complete heart block the continuity of the bundle of His is interrupted and impulses originating from a source above cannot be relayed to the ventricles. Nevertheless the ventricles are still capable of initiating a beat below the block and this intrinsic or idioventricular rate is slower than that from the normal pacemaker, being about 35 beats per minute. It should be observed that the vagus exerts no direct influence on the ventricle. Its action is on the pacemaker and auriculo-ventricular node, and from these sites vagal action is mediated through the bundle of His to the ventricles. The sympathetic nerves on the other hand act directly on the ventricles, as well as through the bundle of His (Best and Taylor, 1952). It follows, therefore, that in complete heart block the ventricles may be free of vagal influence, while the sympathetic nervous system will still exert considerable control. Rowe and White (1958) studied 278 cases of complete heart block. They considered that coronary artery disease with or without hypertension or acute infarction was responsible for 70 per cent of these. The remainder occurred in patients with rheumatic heart disease, congenital heart disease, digitalis poisoning and other less common cardiac ailments. Except in the congenital and digitalis-induced varieties the condition was twice as common in males. In the coronary group the mean survival time was 4 years. StokesAdams attacks occurred in 38 per cent of the group and, rather surprisingly, these cases had the better prognosis. In the congenital group the prognosis is good and symptoms due to heart block are relatively uncommon. STOKES-ADAMS ATTACKS UNDER ANAESTHESIA
Stokes-Adams attacks occurring under anaesthesia have been described by McLemore and Levine (1955), Hodges et al. (1957), Vandam and McLemore (1957) and Zoll (1958). The series reported by Vandam and McLemore of 22 cases of complete heart block included 11 who had suffered Stokes-Adams attacks preoperatively. Of these 11 cases, 5 had Stokes-
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adequate. After 10 minutes the patient began to gag on the endotracheal tube and an attempt was made to increase the ether concentration. The pulse had been continuously monitored and up until this time had been regular and of good quality although still only 38 beats per minute. It now became impalpable and the patient became apnoeic. Absence of the heartbeat was confirmed by auscultation of the praecordium. Anaesthesia was discontinued, hyperventilation with pure oxygen instituted and the head of the table lowered. Thirty seconds later the radial pulse was again palpable, of good volume and regular at 36 beats per minute. Spontaneous respiration recommenced and a mixture of nitrous oxide with oxygen 30 per cent was sufficient to maintain a satisfactory level of anaesthesia. Desloughing was quickly performed but, just after the skin grafts had been cut, cardiac arrest again occurred, heart sounds again being inaudible. The previous regime was again adopted but this time without success. After 80 seconds 3 ml of 1/10.000 adrenaline, previously prepared against such an emergency, was injected into the left ventricle. The heart restarted immediately at a rate of 96 beats per minute and the operation was rapidly concluded. Ephedrine 30 mg was injected intramuscularly and the patient returned to the ward where oxygen was given. He recovered consciousness in 20 minutes and there were no demonstrable sequelae. The pulse reverted to its former rate of 38 per minute.
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BRITISH JOURNAL OF ANAESTHESIA
PRE-OPERATIVE DRUG THERAPY
Digitalis. If cardiac failure is present the use of digitalis is indicated to treat this condition. Conversely if digitalis is responsible for the heart block, withdrawal of the drug will reverse the condition. Atropine. Zoll (1958) recommends the use of atropine 1 mg intravenously as a pre-operative screening test to assess the role, if any, which the vagus may have in the production of the block. If a beneficial result is obtained the use of atropine in a dosage of 1 mg 4-hourly during anaesthesia should be considered. Sympathomimetic drugs. Ephedrine orally or isoprenaline sublingually should be administered to stimulate the idioventricukr centre and abolish the Stokes-Adams attacks if possible. These drugs should be administered in increasing dosage until the desired effect is obtained or toxic symptoms like cerebral irritability, spasm of sphincters, excessive hypertension, or ventricular irritability develop (Zoll, 1958). SUGGESTED ANAESTHETIC MANAGEMENT OF PATIENTS WITH
ESTABLISHED
COMPLETE HEART
BLOCK
Premedication. Vandam and McLemore (1957) suggest that opiates and pethidine cause both central and peripheral circulatory depression and recommend the use of a small dose of a barbiturate. It is, however, probably better to avoid all sedative agents in premedicating these patients. Atropine should be given in therapeutic dosage for its
antisialogogue effect but the administration of large doses, in an attempt to speed up the heart rate, may block the sympathetic ganglia and interfere with sympathetic influences on the ventricular pacemaker (Vandam and McLemore, 1957). Kayden and Stack (1955) have shown that intravenous atropine in complete heart block causes atrial tachycardia but rarely influences the ventricular rate. Nevertheless in cases which on pre-operative testing have shown a beneficial effect to the atropine this should probably be given 4-hourly as suggested by Zoll (1958). Anaesthetic agents. Although ether appears to have been the main anaesthetic agent used, Vandam and McLemore (1957) suggest that the agents are not as important as the skill with which they are used. While this may be so, it is felt that in the possible absence of vagal influence on the ventricle, the use of agents such as cyclopropane, trichloroethylene, chloroform and halothane, which are known to be potentially dangerous in the presence of adrenaline (Wylie and Churchill-Davidson, 1960), may well be equally hazardour i : a situation where the sympathetic nerves alone influence the ventricle. Further proof of this theory is given in a report by Cowan (1954). Here cyclopropane caused ventricular extrasystoles, proceeding to multifocal ventricular tachycardia of 90 per minute, when introduced into an anaesthetic for herniorrhaphy in a patient with complete heart block (anaesthesia had been induced with thiopentone and d-tubocurarine had been used). These undesirable effects disappeared in the reverse order on withdrawing the cyclopropane. A further contraindication to the above agents lies in the fact that if asystole occurs while they are being used, the use of intracardiac adrenaline as a resuscitative measure might precipitate ventricular fibrillation and this would necessitate emergency thoracotomy with its attendant hazards. Complete heart block is usually associated with a marked decrease in cardiac output. Despite an increased stroke volume, the heart cannot increase its rate sufficiently to compensate for this decrease in output (Cecil and Loeb, 1959). The dangers of using thiopentone in these circumstances are well known to all anaesthetists and many will feel it is wise to avoid the use of this
Downloaded from http://bja.oxfordjournals.org/ at New York University on May 31, 2015
Adams attacks during anaesthesia. Of the 11 not suffering Stokes-Adams attacks pre-operatively only 1 had a cardiac arrest preceded by convulsions which occurred during a caudal block and this could have been a toxic reaction to the local anaesthetic. Four of the episodes of cardiac arrest took place before surgery commenced and on two occasions the arrest was associated with endotracheal intubation. The authors suggest as a possible causative mechanism in the latter two cases, laryngeal reflexes, which might not be vagal in origin, quoting King et al. (1951). Thoracotomy was carried out on only one occasion and this could probably have been avoided
GENERAL ANAESTHESIA IN COMPLETE HEART BLOCK drug. If, however, it is used it should be given in dilute solution, slowly and in minimal dosage.
Drug therapy during operation. Should the heart show signs of excessive slowing during the operative procedure, the use of an isoprenaline or adrenaline drip should be considered. Zoll et al. (1958) compared the effects of these two drugs when given by intravenous infusion to twenty-one patients with complete heart block and found that they both have a beneficial effect on the idioventricular pacemaker. Adrenaline tended to cause the blood pressure to rise, while isoprenaline had the opposite effect and they suggested that the level of the blood pressure should determine which one is used. Isoprenaline was infused at a rate of 5 to 43 ^g per minute (mean 12 ^g per minute) and adrenaline at 5 to 44 (Ag per minute (mean 20 jig per minute). Both drugs were given in 1/250,000 solution at an infusion rate of 1 ml/min (approximately 15 drops per minute) and the patient received 4 ^g per minute. The rate of infusion was regulated in accordance with the e.c.g. tracing. They regarded a rise in the idioventricular rate to over 50 beats per minute or premature ventricular beats at an interval of less than 1.2 seconds as potentially toxic manifesta-
tions. Multifocal ventricular rhythm below 50 per minute was ignored as they pointed out that it can occur spontaneously in complete heart block. Drugs such as quinidine and procaine amide should never be given in an attempt to correct any ventricular arrhythmias which may develop during the course of anaesthesia. Paradoxically if ventricular irritability is present, but the basic rhythm is slow, Zoll (1958) recommends the cautious infusion of a sympathomimetic amine in an attempt to accelerate the idioventricular rhythm and thereby abolish the multifocal ventricular irritability. Mechanical means of treatment. Should drug therapy, cither intravenous or intracardiac, be unsuccessful an artificial pacemaker, which can be introduced percutaneously as described by Ross and Harkins (1959), should be available. Briefly this consists of the percutaneous introduction of an active electrode through the chest into the ventricle by means of a No. 16 hollow needle. The needle is first withdrawn and then the electrode is withdrawn until it passes from the cavity of the ventricle into the ventricular muscle mass. The heart should now start to contract at the rate to which the pacemaker has been set. An indifferent electrode is attached to the epigastrium. There is a slight risk of explosion with this apparatus if ether has been in use. It is advisable to have the patient's expirations conducted out of theatre by means of the T-piece described by Bullough in 1954. The latter could at least be available if not actually used during the anaesthetic procedure. If the patient fails to respond to the above regime or ventricular fibrillation ensues, external cardiac massage should be immediately begun (Kouwenhoven, Jude and Knickerbocker, 1960) while preparations are made speedily for thoracotomy with direct cardiac massage and possible electrical defibrillation. SUMMARY
The anaesthetic management of a case of complete heart block with associated Stokes-Adams attacks is described. During nitrous oxide, oxygen and ether anaesthesia administered via an endotracheal tube, two episodes of cardiac arrest occurred. The first was probably associated with
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Muscle relaxants. Gallamine is considered to be the relaxant of choice. The tachycardia which it usually causes is considered undesirable in patients with cardiac disease but this is unlikely to occur in patients with complete heart block as it is due to a vagolytic action identical to that caused by atropine (Riker and Wescoe, 1951). This has already been shown to be unlikely to influence the ventricular rate. The potentiating effect of ether on the myoneural blockade produced by gallamine must be borne in mind. The occasional tendency of d-tubocurarine to cause hypotension (Thomas, 1957) is considered to limit its value in patients with complete heart Mock. Although bradycardia, cardiac arrhythmias ^i i tran 'e:ic cardiac arrest have been reported fo:>".ing intermittent suxamethonium (Bullougli , ^ 5 r : Lupprian and Churchill-Davidson, 19*"'. ?. sLn^c injection of the drug may probably n. j . ~u .* "sly to facilitate endotracheal intubation when tne patient is thereafter being allowed to breathe spontaneously.
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ACKNOWLEDGMENTS
I wish to thank Mr. J. Scott Tough, Regional Consultant in Plastic and Maxillo-Facial Surgery, for
permission to publish the case report; also Dr. J. H. Wright Consultant Physician, Glasgow Royal Infirmary, for permission to reproduce the e.c.g. I would also like to thank Dr. Walter Norris for helpful advice during the preparation of this paper and Miss Janet Chalmers for secretarial help.
REFERENCES
Bencini, A., and Parola, P. L. (1956). "Pneumomassage" of the heart. Surgery, 39, 375. Best, C H., and Taylor, N. B. (1952). The Living Body, 3rd ed., pp. 203, 204. London: Chapman and Hall. Bullough, J. (1954). Anaesthetic explosions: prevention by withdrawal methods. Lancet, 1, 798. (1959). Intermittent suxamethonium injections. Brit. med. J.. 1, 786. Cecil, R. L., and Loeb, R. F. (1959). A Textbook of Medicine, 10th ed., p. 1311. Philadelphia and London: Saunders. Cowan, K. A. (1954). Heart block and cyclopropane. Anaesthesia, 54, 114. Hodges, R. J. H., Witzeman, R. A., and Leigh, M. A. (1957). Multiple Stokes-Adams episodes during anaesthesia. Brit. med. J., 1, 625. Kayden, H. J., and Stack, M. (1955). Studies on complete atrio-ventricular dissociation with special reference to Stokes-Adams syndrome. Abstracted Circulation, 12, 729. King, B. D., Harris, L. C , Greifenstein, F. E., Elder, J. D., and Dripps, R. D. (1951). Reflex circulatory responses to direct laryngoscopy and tracheal intubation performed during general anesthesia. Anesthesiology, 12, 556. Kouwenhoven, W. B., Jude, J. R., and Knickerbocker, G. G. (1960). Closed-chest cardiac massage; /. Amer. med. Ass., 173, 1064. Lupprian, K. G., and Churchill-Davidson, H. C (1960). Effects of suxamethonium on cardiac rhythm. Brit. med. J., 2, 1774. McLemore, G. A., and Levine, S. A. (1955). Possible therapeutic value of cholecystectomy in AdamsStokes disease. Amer. J. med. Sci., 229, 386. Riker, W. F., and Wescoe, W. C. (1951). The pharmacology of Flaxedil with observations on certain analogs. Ann. N.Y. Acad. Sci., 54, 373. Ross, J. K., and Harkins, G. A. (1959). Percutaneous introduction of cardiac pacemaker electrode. Lancet, 2, 1109. Rowe, J. C , and White, P. D. (1958). Complete heart block: a follow-up study. Ann. intern. Med., 49, 260. Thomas, E. T. (1957). The effects of d-tubocurarine on the blood pressure of anaesthetized patients. Lancet, 2, 772. Vandam, L. D., and McLemore, G. A. (1957). Circulatory arrest in patients with complete heart block during anesthesia and surgery. Ann. intern. Med., 47, 518. Wylie, W. D., and Churchill-Davidson, H. G. (1960). A Practice of Anaesthesia, p. 673. London: Lloyd-Luke. Zoll, P. M. U958). Anesthesia in patients with atrioventricular block. Curr. Res. Anesth. Analg., 37, 148. Linenthal, A. J., Gibson, W., Paul. M. H., and Norman, L. R. (1958). Intravenous therapy of Stokes-Adams disease. Circulation, 17, 325.
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mild hypoxia, but there was no obvious reason for the second. The heart was restarted by pneumomassage (hyperventilation of the lungs with oxygen) on the first occasion and by the administration of intracardiac adrenaline on the second. After a search of the literature certain recommendations are made. Atropine 1 mg intravenously is a useful preoperative test to detect the occasional case of complete heart block due to vagal overactivity. Cases which show benefit should be given atropine 1 mg 4-hourly to cover anaesthesia. The pre-operative administration of ephedrine or isoprenaline is recommended until benefit is obtained or toxic reactions to these drugs appear. Digitalis should be used if cardiac failure is present. Some cases of complete heart block are due to digitalis overdose and withdrawal of the drug will cure the condition. In pre-anaesthetic medication depressant drugs like morphine and the barbiturates are best avoided. Atropine should be used as an antisialogogue in appropriate dosage but the use of large doses in an attempt to speed up the ventricular rate may be dangerous. Continuous electrocardiography is mandatory during anaesthesia. Reasons are given for the avoidance of thiopentone, cyclopropane and halogenated hydrocarbons. Minimal ether has certain desirable features, such as its sympathomimetic effects and lack of serialization of the myocardium. A single dose of suxamethonium would appear reasonable to facilitate intubation and gallamine is recommended as the relaxant of choice for intraabdominal procedures or when controlled respiration is indicated. A 1/250,000 solution of adrenaline or isoprenaline should be available to counteract excessive slowing of the heart, the former being preferred if there is associated hypotension and the latter if there is associated hypertension. The cautious infusion of a sympathomimetic amine may abolish multifocal ventricular irritability at slow rates by speeding up the idioventricular rhythm. The use of procaine amide and quinidine should be avoided. The use of percutaneous cardiac pacemaker and closed cardiac massage is discussed.