- Email: [email protected]
Cardiac arrest during anesthesia
Review
Cardiac Arrest during Anesthesia P. FOl?X, DM
All anesthetists and surgeons will, at some time, be faced with the crisis of sudden circulatory collapse due to cardiac arrest occurring in the operating room. Cardiac arrest occurs not only in the elderly and the very sick but also occasionally in the young, fit patient undergoing minor surgery. This is exemplified by the death of a 15year-old girl receiving chloroform anesthesia during the removal of a toenail, reported in the last century by Snow.’ Not infrequently, errors of management can be identified. Thus, in 1948, Macintosh* stated his opinion that anesthetic deaths were preventable and were often due to serious mismanagement of the patient. INCIDENCE, CIRCUMSTANCES AND PROGNOSIS Because of the increased awareness of the possible hazards of anesthesia, safer techniques and agents are continually introduced, and monitoring is becoming more sophisticated. Therefore, the incidence of cardiac arrest should gradually decline. However, comparisons of the incidence of cardiac arrest over the last 30 years do not confirm this expectation. Between 1952 and 1971, the highest reported incidence was one cardiac arrest in 502 administrations of anesthesia,3 and the lowest, one in 4994.4 Between 1972 and 1981, the highest and lowest incidences, respectively, were one in 456 and one in 3808.6 This lack of improvement probably reflects the tendency to accept even the sickest patient for increasingly invasive surgery. Cardiac arrest may occur during all types of surgery but is more frequent during cardiac, thoracic, and major vascular surgery than during other types of surgery.7*8 Over the years, the timing of cardiac arrest has changed. Twenty-five years ago, about a quarter of all
From the Nuffield Department of Anaesthetics, mary, University of Oxford, England. Presented at the First International rest and Resuscitation, Brighton, 1982.
Radcliffe
lnfir-
Conference on Cardiac ArEngland, October 19-21,
Address reprint requests to Dr. Foex, Nuffield Department Anaesthetics, Radcliffe Infirmary, Oxford OX2 6HE, England. Key Words:
Anesthesia,
cardiac
arrest.
of
cardiac arrests relating to anesthesia occurred at induction, approximately one third during maintenance, and about 40% during recovery from anesthesia.9 Because of improved monitoring and better induction agents, the proportion of cardiac arrests occurring at induction has declined to 10%. However, reflecting the greater boldness of both anesthetists and surgeons in operating on very high-risk patients, 64% of cardiac arrests now occur during maintenance of anesthesia. lo Although cardiac arrests in the operating room are witnessed, their prognosis is poor. This is exemplified by a review of 1254 cases by Stoeckel.” In 50% of the cases, resuscitation failed. Another 15% of patients died later of brain anoxia, and a further 20% died of other causes. Only 14% of the patients survived without sequelae. Resuscitation is more likely to be successful when cardiac arrest occurs during elective rather than emergency procedures. l1 The reason for such a low success rate for resuscitation in cases of witnessed cardiac arrest is that 50% of the arrests are due to cardiac standstill, 10% to irreversible myocardial depression, and only 40% to ventricular fibrillation. It is established that resuscitation is less frequently successful when arrest is due to cardiac standstill rather than ventricular fibrillation.‘2,13 CONTRIBUTING FACTORS Factors of risk are very often observed in patients suffering cardiac arrests. Analyzing 95 cases of cardiac arrest, Simmendinger and Torpisch* found evidence of cardiovascular diseases in 58% of the patients. Hypovolemia was present in 25%, diseases of the central nervous system in 20%, respiratory disease in 17%, and other risk factors in 41% of the patients. In only 4% were there no obvious risk factors. Among the cardiovascular diseases, arterial hypertension has been reported in 50%, coronary artery disease in 33%, and cerebrovascular disease in 17% of the patients suffering cardiac arrest during anesthesia and surgery.i4 In the adult, chronic respiratory disease is a risk factor in about 20% of those suffering cardiac arrest.15 In children and infants, respiratory risk factors are as common as cardiac risk factors. The latter are represented by hypovolemia, disorders of kalemia, and 241
AMERICAN
JOURNAL
OF EMERGENCY
MEDICINE
n Volume 2, Number 3 H May 1984
much more rarely by air embolism and cardiac depression due to drug overdosage. CAUSESOFCAROIACAAREST Respiratory Causes Hypoxemia may occur, particularly at induction of anesthesia, because of airway obstruction, inhalation of gastric contents, misplacement of an endotracheal tube, and occasionally because of severe bronchospasm. In children and infants, hypoxemia may develop very rapidly and is often accompanied by severe bradycardia preceding cardiac arrest. Anesthetic agents may cause sufficient respiratory depression to make the patient hypercapnic and hypoxic when ventilation is not controlled and the concentration of the agent is too high. Hypoventilation may be facilitated by posture. Moreover, hypoxemia may occur because of inadvertent administration of hypoxic gas mixtures. The complexity of the anesthetic machine and its associated ventilator makes it possible for hypoxic mixtures to be delivered. Though anesthetic machines should be, and usually are, checked before use, some faults may remain undetected. Alarms for low oxygen concentration in the inspired gas mixture and alarms indicating that ventilation is inadequate because of disconnection should be fitted to anesthetic machines and ventilators. Hypoxemia may also occur because of complications of positive pressure ventilation such as pneumothorax and pneumomediastinum, which severely compromise the circulation. Usually, moderate hypoxemia causes sympathetic stimulation, tachycardia, and hypertension. However, more severe hypoxemia causes vagal stimulation, with bradycardia and hypotension, which usually precede cardiac arrest. Hypercarbia, caused by insufficient alveolar ventilation, causes sympathetic overactivity and facilitates the development of dysrhythmias, which in turn may cause cardiac arrest. Cardiac Causes Coronary artery disease is frequently found in patients who have experienced cardiac arrest. Very often, when resuscitation has been ineffective, postmortem examination shows that severe coronary artery lesions were present.16 Arterial hypertension is also a cause of sudden death;” not surprisingly, it is frequently present in patients who have suffered cardiac arrest during anesthesia and surgery. Not infrequently, the severity of the coronary heart disease is underestimated during the routine preoperative assessment. Even recent myocardial infarction may be overlooked if it has been muted or silent. In 242
these patients the risk of reinfarction and death is very high.i8 Unstable angina may remain undiagnosed as such. Patients with poor ventricular function and even ventricular aneurysms are not always identified. In these patients anesthesia and surgery may cause severe cardiac depression leading to cardiac arrest. Disorders of atrioventricular or intraventricular conduction may be substantially exacerbated by anesthesia and result in cardiac arrest. There are several reasons for the worsening of conduction. Anesthetic agents may reduce atrioventricular conduction, and they have an additive effect to that of antiarrhythmic agents such as the slow calcium channel blockers. Anesthesia with some volatile agents may sensitize the myocardium to the arrhythmogenic effect of the catecholamines. This results in ectopic rhythms, which may transform a mild degree of heart block into complete heart block. Alterations of potassium ion concentration frequently occur in the perioperative period, facilitating ectopic rhythms and, therefore, heart block. If conduction disorders are overlooked, it is likely that patients in whom a temporary pacemaker is required will not benefit from this type of protection, and avoidable deaths will ensue. The indication for temporary pacing is almost absolute for third degree and Mobitz type II blocks. In other blocks, including the bifascicular blocks, temporary pacing is imperative if the patients have undergone Stokes-Adams attacks. Temporary pacing is also indicated in case of severe bradycardia accompanied by cardiac failure, angina, or syncope: atria1 fibrillation with very slow ventricular rate; and sick sinus syndrome. Other cardiac or circulatory causes of cardiac arrest include all types of restrictions imposed on the circulation by hypovolemia (often made worse by intermittent positive pressure ventilation), embolization (thrombus, air, fat, amniotic fluid), constrictive pericarditis, and cardiac tamponade. In all of these conditions the effective circulating volume is reduced, coronary perfusion is compromised, and cardiac arrest may suddenly occur. It must be remembered that most anesthetic agents cause myocardial depression; this is more pronounced with the volatile anesthetics than with the narcotics. Accidental overdosage may cause cardiac arrest. However, when the myocardium is compromised, even conventional doses of most anesthetics may produce marked cardiac depression. Cardiac arrests may also occur because of metabolic disorders, particularly abnormalities of kalemia or calcemia, which can be induced by massive blood transfusion or infusion of crystalloids, or facilitated by respiratory or metabolic acid-base disorders. Cardiac arrests may relate directly to the use of drugs that are necessary for anesthesia and surgery. Besides the anesthetic agents themselves, other drugs
FOEX n CARDIAC
are required for the treatment of many patients, especially the muscle relaxants. The depolarizing muscle relaxant succinylcholine may cause severe bradycardia, and many cardiac arrests have been reported, especially when more than one dose has been used. In patients with renal failure, spinal injury, burns, and muscular dystrophy, succinylcholine can cause severe hyperkalemia and cardiac arrest. With the non-depolarizing muscle relaxants (d-tubocurarine, synthetic curare), there is the possibility of histamine release accompanied by hypotension and tachycardia. When the effects of the non-depolarizing muscle relaxants are reversed by the administration of atropine and neostigmine, severe bradycardia may occur and cardiac arrests have been observed. Interactions between anesthetic agents and cardiovascular drugs may occur. The arrhythmogenic effect of the catecholamines is potentiated by the volatile anesthetics. Myocardial depression and slowing of atrioventricular conduction, which characterize the administration of slow calcium channel blockers, are exaggerated by volatile anesthetics. l9 Severe hypertensive crises followed by circulatory collapse have been described in patients receiving monoamino oxidase inhibitors. Severe dysrhythmias have been reported in patients treated with tricyclic antidepressants. Special techniques such as deliberately induced hypotension and hypothermia may cause marked alterations of the circulation accompanied by dysrhythmias and, on occasion, cardiac arrest. With the introduction of more sophisticated monitoring, more equipment is directly in contact with the patient, and electric shocks can be delivered by small leakage of current and cause cardiac arrest. Local and regional anesthesia are not without risk. With local anesthesia, excessive doses of the agent may cause dysrhythmias, seizures, and acute circulatory failure. Regional anesthesia (spinal and epidural anesthesia) requires smaller doses of local anesthetics but often causes substantial vasodilatation accompanied by hypotension and, on occasion, circulatory collapse. CARDIACARRESTATTRIBUTEDTO ANESTHESIA For many years, a bias has prevailed in all studies of morbidity and mortality of anesthesia. Anesthesia has been considered responsible for the complications only when there had been technical error, inadequate assessment, or departure from accepted practice. Thus, in most series of cardiac arrests, only a small proportion is attributed solely to anesthesia. The proportion varies between 22%20 and 30%.21 The majority of arrests are considered to be secondary to the surgical procedure or to associated medical conditions.
ARREST
DURING ANESTHESIA
The same bias prevailed in the recent study of mortality of anesthesia by the Association of Anaesthetists of Great Britain and Ireland.22 Only a small proportion of postoperative deaths were examined in detail when either anesthetist or surgeon felt that anesthesia might have contributed to the deaths. With this approach, most of the deaths attributed to anesthesia were due to errors in management. In the series reported by the Subcommittee on Mortality of Anesthesia (South Australia), more than four errors were detected in each case.‘O This is why, 30 years after Macintosh’s statement that anesthetic deaths were preventable, Lauwers wrote that anesthetic deaths were due to ignorance, negligence, and only rarely to inadequate scientific knowledge. 23 This attitude has been challenged,24 and it is likely that scientific inadequacies play a greater role than has usually been accepted. CAN ANESTHESIADAMAGETHE HEART? Our present knowledge of the effects of anesthesia on the heart and the circulation is fairly extensive but is far from complete. Most of the experimental work carried out in the past used the normal heart as the model, and relatively little is known of the effects of anesthesia on the ischemic myocardium. There have been studies of the effects of anesthetic agents on myocardium rendered acutely ischemic by the complete or almost complete occlusion of a coronary artery.25-28 In these studies, anesthesia appeared to reduce the extent of the ischemic damage, ostensibly by improving the ratio between oxygen supply and oxygen demand. 29 In all of these studies, the anesthetic agent under investigation caused such reductions in arterial pressure and in heart rate that myocardial oxygen demand was reduced. The limitations of these studies is that they mimic the condition of an acute myocardial infarction and not that of a compromised coronary circulation. Recently, the effects of halothane and enflurane on global and regional cardiac function have been studied in dogs in which a coronary artery had been critically narrowed but not occ1uded.30-32 When critical constriction is applied, the coronary artery caliber is reduced, autoregulation is abolished, and there is no coronary flow reserve. 33,34Under the two volatile agents studied, coronary blood flow was reduced by about 20% by critical constriction.31,32 Coronary flow in the compromised myocardium would appear to be comparable to that in an area causing angina pectoris. In such an area, coronary blood flow is able to meet basal oxygen demands, cannot increase sufficiently in response to stresses that increase oxygen consumption, and is severely compromised when the coronary perfusion pressure decreases. With this model of critical constriction, increasing the inspired concentration of 243
AMERICAN
JOURNAL
OF EMERGENCY
MEDICINE
n Volume 2, Number 3 H May 1984
halothane or enflurane caused greater depression of myocardium supplied by a narrowed coronary artery than of normal myocardium. Moreover, abnormal patterns of wall motion were observed in the compromised territory.31 These abnormal patterns of wall function were similar to those observed in myocardial ischemia34 and reflected the severe reduction in coronary blood flow caused by the dose-dependent reductions in arterial pressure that followed the administration of increasing concentrations of the agent.31.32 Studies of the effects of anesthesia on myocardial wall function and on the true incidence of ischemic episodes during surgery are under way. In a study of 24 patients with coronary artery disease, abnormalities of left ventricular wall function, detected by echocardiography, were observed in ten patients. In only one patient were the ST segments abnormal.3s In patients with coronary artery disease, anesthesia with isoflurane has been shown to cause ischemic changes of ST segments.36 No such changes were observed in patients receiving halothane anesthesia.37 However, it is now demonstrated that routine monitoring of the electrocardiogram as practiced during anesthesia reveals only a very small proportion of the episodes of myocardial ischemia.38 Transient ischemia is known to occur after laryngoscopy and endotracheal intubation, as well as during any episodes of sympathetic overactivity.39 While ischemia is usually transient, it can be accompanied by more prolonged reductions in ejection fraction4* indicating that the myocardium has been severely compromised. It must be remembered that transient episodes of ischemia may cause abnormalities of cellular myocardial metabolism, ultrastructure, and function that last for several days after reperfusion.41 Thus, episodes of myocardial ischemia occurring during anesthesia and surgery may remain undetected by routine monitoring and yet cause alterations in the myocardium that last for several hours or days and could therefore contribute to the cardiovascular complications of anesthesia and surgery, including cardiac arrest. Cardiac arrest may well occur not only because of incompetence and negligence, but because of scientific inadequacies, more often than is usually accepted. Anesthesia, conducted according to conventional and well-accepted practice, may exert marked effects on the compromised myocardium and therefore, without any fault on the anesthetist’s part, facilitate the development of cardiovascular complications of surgery. There is a need for better means of detection of myocardial ischemia, for aggressive treatment of abnormalities of the circulation that may facilitate myocardial ischemia, and for extensive investigation of the place of cardiovascular drugs, i.e., beta-adrenergic blockers, calcium influx blockers, and nitrates, in pro244
tecting the myocardium against the adverse effects anesthesia may have in the compromised heart. REFERENCES 1. Snow J. On chloroform and other anaesthetics. London: J Churchill, 1858. R. Deaths under anaesthetics. Br J Anaesth 2. Macintosh 1948;21:107-136. 3. Bodlander FMS. Deaths associated with anaesthesia. Br J Anaesth 1975;47:36-40. 4. Memery HN. Anesthesia mortality in private practice. JAMA 1965;194:1185-1188. 5. Harrison GG. Death attributable to anaesthesia. Br J Anaesth 1978;50:1041-1046. 6. Hovi-Viander M. Deaths associated with anaesthesia in Finland. Br J Anaesth 1980;52:483-489. 7. Huguenard P, Jacquenoud P, Picard JM. L’arret cardiaque en anesthesie-reanimation. In Problemes de reanimation (5= serie). Paris: S.P.E.I., 1968. 8. Simmendinger HJ, Torpisch P. Der Herz-Kreislauf Stillstand im Operationsaal: Eine analyse von 95 Fallen. Z Prakt Anasthesiol 1973;8:288-293. 9. Edwards G, Morton HJV, Pask EA, Wylie WD. Deaths associated with anaesthesia: A report on 1,000 cases. Anaesthesia 1956;2:194-220. 10. Special committee investigating death under anaesthesia. Report on 745 classified cases: 1960-1968. Med J Australia 1970;1:573-594. 11. Stoeckel H. Ergebnisse kardiozirkulatorischer Wiederbelebung. Z Prakt Anasthesiol 1969;4:184-200. 12. Scott RPF. Cardiopulmonary resuscitation in a teaching hospital: A survey of cardiac arrests occurring outside intensive care units and emergency rooms. Anaesthesia 1981;36:526-530. 13. Wildsmith JAW, Dennyson WG, Myers KW. Results of resuscitation following cardiac arrest: A review from a major teaching hospital. Br J Anaesth 1972;44:716-720. 14. McClure JN Jr, Skardasis GM, Brown JM. Cardiac arrest in the operating area. Am Surg 1972;38:241-246. 15. Salem MR, Bennett EJ, Schweiss JF, et al. Cardiac arrest related to anesthesia: Contributing factors in infants and children. JAMA 1975;233:238-241. 16. Roberts WC, Jones AA. Quantitation of coronary arterial narrowing at necropsy in sudden cardiac death. Am J Cardiol 1979;44:39-45. 17. Anderson KR. Hypertension and sudden cardiac death. NZ Med J 1982;1:33-34. 18. Steen PA, Tinker JH, Tarhan S. Myocardial reinfarction after anesthesia and surgery. JAMA 1978;239:2586-2570. 19. Kapur PA, Flacke WE. Epinephrine-induced arrhythmias and cardiovascular function after verapamil during halothane anesthesia in the dog. Anesthesiology 1981; 55:218-225. 20. Taylor G, Larson CP, Prestwich R. Unexpected cardiac arrest during anesthesia and surgery. JAMA 1976; 236:2758-2760. 21. Baraka A. Anesthetic mortality. Anesthesiology 1980; 52:283-284. 22. Lunn JN, Mushin WW. Mortality associated with anaesthesia. London: Nuffield Provincial Hospitals Trust, 1982:104. 23. Lauwers P. Anesthetic death. Acta Anaesth Belg 1978;29:19-28. 24. Keats AS. What do we know about anesthetic mortality. Anesthesiology 1979;50:387-392.
FOEX n CARDIAC ARREST DURING ANESTHESIA
25. Bland JHK, Lowenstein E. Halothane induced decrease in experimental myocardial ischemia in non-failing canine heart. Anesthesiology 1976;45:267-293. 26. Ribeiro LGT, Yasuda T, Lowenstein E, et al. Comparative effects on anatomic infarct size of verapamil, ibuprofen, and morphine-promethazine-chlorpromazine combination. Am J Cardiol 1979;43:396. 27. Davis RF, DeBoer LWV, Rude RE, et al. Beneficial effects of halothane anesthesia on myocardial infarction size in dogs. Crit Care Med 1979;7:134. 26. Van Ackern K, Mittmann U, Bruckner UB, et al. Concept in patients with hypertension and coronary heart disease: Clinical and experimental aspects. In Peter K, Jeoch F (eds). Anaesthesia Today and Tomorrow. Berlin: Springer-Verlag, 1962:205-216. 29. Smith G, Rogers K, Thorburn J. Halothane improves the balance of oxygen supply to demand in acute experimental myocardial ischaemia. Br J Anaesth 1980;52:577583. 30. Lowenstein E, Foex P, Francis CM, et al. Regional ischemic ventricular dysfunction in myocardium supplied by a narrowed coronary artery with increasing halothane concentration in the dog. Anesthesiology 1981;55:349-359. 31. Francis CM, Foex P, Lowenstein E, et al. Interaction between regional myocardial ischaemia and left ventricular performance under halothane anaesthesia. Br J Anaesth 1982;54:965-980. 32. Cutfield GR, Francis CM, Foex P, et al. Myocardial function and critical constriction of the left anterior descending coronary artery: Effects of enflurane. Br J Anaesth 1980;52:953P.
33. Elzinga WE, Skinner DB. Hemodynamic characteristics of critical stenosis in canine coronary arteries. J Thorac Cardiovasc Surg 1975;69:217-222. 34. Hagl S, Heimisch W, Meisner H, et al. The effect of hemodilution on regional myocardial function in the presence of coronary stenosis. Basic Res Cardiol 1977;72:344-364. 35. Elliott PL, Schauble JF, Weiss J, et al. Echocardiography and LV function during anesthesia. Anesthesiology 1980;53:S105. 36. Reiz S, Balfors E, et al. Isoflurane: a powerful coronary vasodilator in patients with coronary artery disease. Anesthesiology 1983;59:91-97. 37. Reiz S, Balfors E, Gustavsson B, et al. Effects of halothane on coronary haemodynamics and myocardial metabolism in patients with ischemic heart disease and heart failure. Acta Anaesth Stand 1982;26:133-138. 38. Roy WL, Edelist G, Gilbert B. Myocardial ischemia during non-cardiac surgery procedures in patients with coronary artery disease. Anesthesiology 1979;51:393-397. 39. Prys-Roberts C, Greene LT, Meloche R, et al. Studies of anaesthesia in relation to hypertension: II. Haemodynamic consequences of induction and endotracheal intubation. Br J Anaesth 1971;43:531-547. 40. Giles RW, Berger HJ, Barash PG, et al. Continuous monitoring of left ventricular performance with the computerized nuclear probe during laryngoscopy and intubation before coronary artery bypass surgery. Am J Cardiol 1982;50:735-741. 41. Braunwald E, Kloner RA. The stunned myocardium-prolonged postischemic ventricular dysfunction. Circulation 1982;66:1146-1149.
245
Cardiac Arrest during Anesthesia P. FOl?X, DM
All anesthetists and surgeons will, at some time, be faced with the crisis of sudden circulatory collapse due to cardiac arrest occurring in the operating room. Cardiac arrest occurs not only in the elderly and the very sick but also occasionally in the young, fit patient undergoing minor surgery. This is exemplified by the death of a 15year-old girl receiving chloroform anesthesia during the removal of a toenail, reported in the last century by Snow.’ Not infrequently, errors of management can be identified. Thus, in 1948, Macintosh* stated his opinion that anesthetic deaths were preventable and were often due to serious mismanagement of the patient. INCIDENCE, CIRCUMSTANCES AND PROGNOSIS Because of the increased awareness of the possible hazards of anesthesia, safer techniques and agents are continually introduced, and monitoring is becoming more sophisticated. Therefore, the incidence of cardiac arrest should gradually decline. However, comparisons of the incidence of cardiac arrest over the last 30 years do not confirm this expectation. Between 1952 and 1971, the highest reported incidence was one cardiac arrest in 502 administrations of anesthesia,3 and the lowest, one in 4994.4 Between 1972 and 1981, the highest and lowest incidences, respectively, were one in 456 and one in 3808.6 This lack of improvement probably reflects the tendency to accept even the sickest patient for increasingly invasive surgery. Cardiac arrest may occur during all types of surgery but is more frequent during cardiac, thoracic, and major vascular surgery than during other types of surgery.7*8 Over the years, the timing of cardiac arrest has changed. Twenty-five years ago, about a quarter of all
From the Nuffield Department of Anaesthetics, mary, University of Oxford, England. Presented at the First International rest and Resuscitation, Brighton, 1982.
Radcliffe
lnfir-
Conference on Cardiac ArEngland, October 19-21,
Address reprint requests to Dr. Foex, Nuffield Department Anaesthetics, Radcliffe Infirmary, Oxford OX2 6HE, England. Key Words:
Anesthesia,
cardiac
arrest.
of
cardiac arrests relating to anesthesia occurred at induction, approximately one third during maintenance, and about 40% during recovery from anesthesia.9 Because of improved monitoring and better induction agents, the proportion of cardiac arrests occurring at induction has declined to 10%. However, reflecting the greater boldness of both anesthetists and surgeons in operating on very high-risk patients, 64% of cardiac arrests now occur during maintenance of anesthesia. lo Although cardiac arrests in the operating room are witnessed, their prognosis is poor. This is exemplified by a review of 1254 cases by Stoeckel.” In 50% of the cases, resuscitation failed. Another 15% of patients died later of brain anoxia, and a further 20% died of other causes. Only 14% of the patients survived without sequelae. Resuscitation is more likely to be successful when cardiac arrest occurs during elective rather than emergency procedures. l1 The reason for such a low success rate for resuscitation in cases of witnessed cardiac arrest is that 50% of the arrests are due to cardiac standstill, 10% to irreversible myocardial depression, and only 40% to ventricular fibrillation. It is established that resuscitation is less frequently successful when arrest is due to cardiac standstill rather than ventricular fibrillation.‘2,13 CONTRIBUTING FACTORS Factors of risk are very often observed in patients suffering cardiac arrests. Analyzing 95 cases of cardiac arrest, Simmendinger and Torpisch* found evidence of cardiovascular diseases in 58% of the patients. Hypovolemia was present in 25%, diseases of the central nervous system in 20%, respiratory disease in 17%, and other risk factors in 41% of the patients. In only 4% were there no obvious risk factors. Among the cardiovascular diseases, arterial hypertension has been reported in 50%, coronary artery disease in 33%, and cerebrovascular disease in 17% of the patients suffering cardiac arrest during anesthesia and surgery.i4 In the adult, chronic respiratory disease is a risk factor in about 20% of those suffering cardiac arrest.15 In children and infants, respiratory risk factors are as common as cardiac risk factors. The latter are represented by hypovolemia, disorders of kalemia, and 241
AMERICAN
JOURNAL
OF EMERGENCY
MEDICINE
n Volume 2, Number 3 H May 1984
much more rarely by air embolism and cardiac depression due to drug overdosage. CAUSESOFCAROIACAAREST Respiratory Causes Hypoxemia may occur, particularly at induction of anesthesia, because of airway obstruction, inhalation of gastric contents, misplacement of an endotracheal tube, and occasionally because of severe bronchospasm. In children and infants, hypoxemia may develop very rapidly and is often accompanied by severe bradycardia preceding cardiac arrest. Anesthetic agents may cause sufficient respiratory depression to make the patient hypercapnic and hypoxic when ventilation is not controlled and the concentration of the agent is too high. Hypoventilation may be facilitated by posture. Moreover, hypoxemia may occur because of inadvertent administration of hypoxic gas mixtures. The complexity of the anesthetic machine and its associated ventilator makes it possible for hypoxic mixtures to be delivered. Though anesthetic machines should be, and usually are, checked before use, some faults may remain undetected. Alarms for low oxygen concentration in the inspired gas mixture and alarms indicating that ventilation is inadequate because of disconnection should be fitted to anesthetic machines and ventilators. Hypoxemia may also occur because of complications of positive pressure ventilation such as pneumothorax and pneumomediastinum, which severely compromise the circulation. Usually, moderate hypoxemia causes sympathetic stimulation, tachycardia, and hypertension. However, more severe hypoxemia causes vagal stimulation, with bradycardia and hypotension, which usually precede cardiac arrest. Hypercarbia, caused by insufficient alveolar ventilation, causes sympathetic overactivity and facilitates the development of dysrhythmias, which in turn may cause cardiac arrest. Cardiac Causes Coronary artery disease is frequently found in patients who have experienced cardiac arrest. Very often, when resuscitation has been ineffective, postmortem examination shows that severe coronary artery lesions were present.16 Arterial hypertension is also a cause of sudden death;” not surprisingly, it is frequently present in patients who have suffered cardiac arrest during anesthesia and surgery. Not infrequently, the severity of the coronary heart disease is underestimated during the routine preoperative assessment. Even recent myocardial infarction may be overlooked if it has been muted or silent. In 242
these patients the risk of reinfarction and death is very high.i8 Unstable angina may remain undiagnosed as such. Patients with poor ventricular function and even ventricular aneurysms are not always identified. In these patients anesthesia and surgery may cause severe cardiac depression leading to cardiac arrest. Disorders of atrioventricular or intraventricular conduction may be substantially exacerbated by anesthesia and result in cardiac arrest. There are several reasons for the worsening of conduction. Anesthetic agents may reduce atrioventricular conduction, and they have an additive effect to that of antiarrhythmic agents such as the slow calcium channel blockers. Anesthesia with some volatile agents may sensitize the myocardium to the arrhythmogenic effect of the catecholamines. This results in ectopic rhythms, which may transform a mild degree of heart block into complete heart block. Alterations of potassium ion concentration frequently occur in the perioperative period, facilitating ectopic rhythms and, therefore, heart block. If conduction disorders are overlooked, it is likely that patients in whom a temporary pacemaker is required will not benefit from this type of protection, and avoidable deaths will ensue. The indication for temporary pacing is almost absolute for third degree and Mobitz type II blocks. In other blocks, including the bifascicular blocks, temporary pacing is imperative if the patients have undergone Stokes-Adams attacks. Temporary pacing is also indicated in case of severe bradycardia accompanied by cardiac failure, angina, or syncope: atria1 fibrillation with very slow ventricular rate; and sick sinus syndrome. Other cardiac or circulatory causes of cardiac arrest include all types of restrictions imposed on the circulation by hypovolemia (often made worse by intermittent positive pressure ventilation), embolization (thrombus, air, fat, amniotic fluid), constrictive pericarditis, and cardiac tamponade. In all of these conditions the effective circulating volume is reduced, coronary perfusion is compromised, and cardiac arrest may suddenly occur. It must be remembered that most anesthetic agents cause myocardial depression; this is more pronounced with the volatile anesthetics than with the narcotics. Accidental overdosage may cause cardiac arrest. However, when the myocardium is compromised, even conventional doses of most anesthetics may produce marked cardiac depression. Cardiac arrests may also occur because of metabolic disorders, particularly abnormalities of kalemia or calcemia, which can be induced by massive blood transfusion or infusion of crystalloids, or facilitated by respiratory or metabolic acid-base disorders. Cardiac arrests may relate directly to the use of drugs that are necessary for anesthesia and surgery. Besides the anesthetic agents themselves, other drugs
FOEX n CARDIAC
are required for the treatment of many patients, especially the muscle relaxants. The depolarizing muscle relaxant succinylcholine may cause severe bradycardia, and many cardiac arrests have been reported, especially when more than one dose has been used. In patients with renal failure, spinal injury, burns, and muscular dystrophy, succinylcholine can cause severe hyperkalemia and cardiac arrest. With the non-depolarizing muscle relaxants (d-tubocurarine, synthetic curare), there is the possibility of histamine release accompanied by hypotension and tachycardia. When the effects of the non-depolarizing muscle relaxants are reversed by the administration of atropine and neostigmine, severe bradycardia may occur and cardiac arrests have been observed. Interactions between anesthetic agents and cardiovascular drugs may occur. The arrhythmogenic effect of the catecholamines is potentiated by the volatile anesthetics. Myocardial depression and slowing of atrioventricular conduction, which characterize the administration of slow calcium channel blockers, are exaggerated by volatile anesthetics. l9 Severe hypertensive crises followed by circulatory collapse have been described in patients receiving monoamino oxidase inhibitors. Severe dysrhythmias have been reported in patients treated with tricyclic antidepressants. Special techniques such as deliberately induced hypotension and hypothermia may cause marked alterations of the circulation accompanied by dysrhythmias and, on occasion, cardiac arrest. With the introduction of more sophisticated monitoring, more equipment is directly in contact with the patient, and electric shocks can be delivered by small leakage of current and cause cardiac arrest. Local and regional anesthesia are not without risk. With local anesthesia, excessive doses of the agent may cause dysrhythmias, seizures, and acute circulatory failure. Regional anesthesia (spinal and epidural anesthesia) requires smaller doses of local anesthetics but often causes substantial vasodilatation accompanied by hypotension and, on occasion, circulatory collapse. CARDIACARRESTATTRIBUTEDTO ANESTHESIA For many years, a bias has prevailed in all studies of morbidity and mortality of anesthesia. Anesthesia has been considered responsible for the complications only when there had been technical error, inadequate assessment, or departure from accepted practice. Thus, in most series of cardiac arrests, only a small proportion is attributed solely to anesthesia. The proportion varies between 22%20 and 30%.21 The majority of arrests are considered to be secondary to the surgical procedure or to associated medical conditions.
ARREST
DURING ANESTHESIA
The same bias prevailed in the recent study of mortality of anesthesia by the Association of Anaesthetists of Great Britain and Ireland.22 Only a small proportion of postoperative deaths were examined in detail when either anesthetist or surgeon felt that anesthesia might have contributed to the deaths. With this approach, most of the deaths attributed to anesthesia were due to errors in management. In the series reported by the Subcommittee on Mortality of Anesthesia (South Australia), more than four errors were detected in each case.‘O This is why, 30 years after Macintosh’s statement that anesthetic deaths were preventable, Lauwers wrote that anesthetic deaths were due to ignorance, negligence, and only rarely to inadequate scientific knowledge. 23 This attitude has been challenged,24 and it is likely that scientific inadequacies play a greater role than has usually been accepted. CAN ANESTHESIADAMAGETHE HEART? Our present knowledge of the effects of anesthesia on the heart and the circulation is fairly extensive but is far from complete. Most of the experimental work carried out in the past used the normal heart as the model, and relatively little is known of the effects of anesthesia on the ischemic myocardium. There have been studies of the effects of anesthetic agents on myocardium rendered acutely ischemic by the complete or almost complete occlusion of a coronary artery.25-28 In these studies, anesthesia appeared to reduce the extent of the ischemic damage, ostensibly by improving the ratio between oxygen supply and oxygen demand. 29 In all of these studies, the anesthetic agent under investigation caused such reductions in arterial pressure and in heart rate that myocardial oxygen demand was reduced. The limitations of these studies is that they mimic the condition of an acute myocardial infarction and not that of a compromised coronary circulation. Recently, the effects of halothane and enflurane on global and regional cardiac function have been studied in dogs in which a coronary artery had been critically narrowed but not occ1uded.30-32 When critical constriction is applied, the coronary artery caliber is reduced, autoregulation is abolished, and there is no coronary flow reserve. 33,34Under the two volatile agents studied, coronary blood flow was reduced by about 20% by critical constriction.31,32 Coronary flow in the compromised myocardium would appear to be comparable to that in an area causing angina pectoris. In such an area, coronary blood flow is able to meet basal oxygen demands, cannot increase sufficiently in response to stresses that increase oxygen consumption, and is severely compromised when the coronary perfusion pressure decreases. With this model of critical constriction, increasing the inspired concentration of 243
AMERICAN
JOURNAL
OF EMERGENCY
MEDICINE
n Volume 2, Number 3 H May 1984
halothane or enflurane caused greater depression of myocardium supplied by a narrowed coronary artery than of normal myocardium. Moreover, abnormal patterns of wall motion were observed in the compromised territory.31 These abnormal patterns of wall function were similar to those observed in myocardial ischemia34 and reflected the severe reduction in coronary blood flow caused by the dose-dependent reductions in arterial pressure that followed the administration of increasing concentrations of the agent.31.32 Studies of the effects of anesthesia on myocardial wall function and on the true incidence of ischemic episodes during surgery are under way. In a study of 24 patients with coronary artery disease, abnormalities of left ventricular wall function, detected by echocardiography, were observed in ten patients. In only one patient were the ST segments abnormal.3s In patients with coronary artery disease, anesthesia with isoflurane has been shown to cause ischemic changes of ST segments.36 No such changes were observed in patients receiving halothane anesthesia.37 However, it is now demonstrated that routine monitoring of the electrocardiogram as practiced during anesthesia reveals only a very small proportion of the episodes of myocardial ischemia.38 Transient ischemia is known to occur after laryngoscopy and endotracheal intubation, as well as during any episodes of sympathetic overactivity.39 While ischemia is usually transient, it can be accompanied by more prolonged reductions in ejection fraction4* indicating that the myocardium has been severely compromised. It must be remembered that transient episodes of ischemia may cause abnormalities of cellular myocardial metabolism, ultrastructure, and function that last for several days after reperfusion.41 Thus, episodes of myocardial ischemia occurring during anesthesia and surgery may remain undetected by routine monitoring and yet cause alterations in the myocardium that last for several hours or days and could therefore contribute to the cardiovascular complications of anesthesia and surgery, including cardiac arrest. Cardiac arrest may well occur not only because of incompetence and negligence, but because of scientific inadequacies, more often than is usually accepted. Anesthesia, conducted according to conventional and well-accepted practice, may exert marked effects on the compromised myocardium and therefore, without any fault on the anesthetist’s part, facilitate the development of cardiovascular complications of surgery. There is a need for better means of detection of myocardial ischemia, for aggressive treatment of abnormalities of the circulation that may facilitate myocardial ischemia, and for extensive investigation of the place of cardiovascular drugs, i.e., beta-adrenergic blockers, calcium influx blockers, and nitrates, in pro244
tecting the myocardium against the adverse effects anesthesia may have in the compromised heart. REFERENCES 1. Snow J. On chloroform and other anaesthetics. London: J Churchill, 1858. R. Deaths under anaesthetics. Br J Anaesth 2. Macintosh 1948;21:107-136. 3. Bodlander FMS. Deaths associated with anaesthesia. Br J Anaesth 1975;47:36-40. 4. Memery HN. Anesthesia mortality in private practice. JAMA 1965;194:1185-1188. 5. Harrison GG. Death attributable to anaesthesia. Br J Anaesth 1978;50:1041-1046. 6. Hovi-Viander M. Deaths associated with anaesthesia in Finland. Br J Anaesth 1980;52:483-489. 7. Huguenard P, Jacquenoud P, Picard JM. L’arret cardiaque en anesthesie-reanimation. In Problemes de reanimation (5= serie). Paris: S.P.E.I., 1968. 8. Simmendinger HJ, Torpisch P. Der Herz-Kreislauf Stillstand im Operationsaal: Eine analyse von 95 Fallen. Z Prakt Anasthesiol 1973;8:288-293. 9. Edwards G, Morton HJV, Pask EA, Wylie WD. Deaths associated with anaesthesia: A report on 1,000 cases. Anaesthesia 1956;2:194-220. 10. Special committee investigating death under anaesthesia. Report on 745 classified cases: 1960-1968. Med J Australia 1970;1:573-594. 11. Stoeckel H. Ergebnisse kardiozirkulatorischer Wiederbelebung. Z Prakt Anasthesiol 1969;4:184-200. 12. Scott RPF. Cardiopulmonary resuscitation in a teaching hospital: A survey of cardiac arrests occurring outside intensive care units and emergency rooms. Anaesthesia 1981;36:526-530. 13. Wildsmith JAW, Dennyson WG, Myers KW. Results of resuscitation following cardiac arrest: A review from a major teaching hospital. Br J Anaesth 1972;44:716-720. 14. McClure JN Jr, Skardasis GM, Brown JM. Cardiac arrest in the operating area. Am Surg 1972;38:241-246. 15. Salem MR, Bennett EJ, Schweiss JF, et al. Cardiac arrest related to anesthesia: Contributing factors in infants and children. JAMA 1975;233:238-241. 16. Roberts WC, Jones AA. Quantitation of coronary arterial narrowing at necropsy in sudden cardiac death. Am J Cardiol 1979;44:39-45. 17. Anderson KR. Hypertension and sudden cardiac death. NZ Med J 1982;1:33-34. 18. Steen PA, Tinker JH, Tarhan S. Myocardial reinfarction after anesthesia and surgery. JAMA 1978;239:2586-2570. 19. Kapur PA, Flacke WE. Epinephrine-induced arrhythmias and cardiovascular function after verapamil during halothane anesthesia in the dog. Anesthesiology 1981; 55:218-225. 20. Taylor G, Larson CP, Prestwich R. Unexpected cardiac arrest during anesthesia and surgery. JAMA 1976; 236:2758-2760. 21. Baraka A. Anesthetic mortality. Anesthesiology 1980; 52:283-284. 22. Lunn JN, Mushin WW. Mortality associated with anaesthesia. London: Nuffield Provincial Hospitals Trust, 1982:104. 23. Lauwers P. Anesthetic death. Acta Anaesth Belg 1978;29:19-28. 24. Keats AS. What do we know about anesthetic mortality. Anesthesiology 1979;50:387-392.
FOEX n CARDIAC ARREST DURING ANESTHESIA
25. Bland JHK, Lowenstein E. Halothane induced decrease in experimental myocardial ischemia in non-failing canine heart. Anesthesiology 1976;45:267-293. 26. Ribeiro LGT, Yasuda T, Lowenstein E, et al. Comparative effects on anatomic infarct size of verapamil, ibuprofen, and morphine-promethazine-chlorpromazine combination. Am J Cardiol 1979;43:396. 27. Davis RF, DeBoer LWV, Rude RE, et al. Beneficial effects of halothane anesthesia on myocardial infarction size in dogs. Crit Care Med 1979;7:134. 26. Van Ackern K, Mittmann U, Bruckner UB, et al. Concept in patients with hypertension and coronary heart disease: Clinical and experimental aspects. In Peter K, Jeoch F (eds). Anaesthesia Today and Tomorrow. Berlin: Springer-Verlag, 1962:205-216. 29. Smith G, Rogers K, Thorburn J. Halothane improves the balance of oxygen supply to demand in acute experimental myocardial ischaemia. Br J Anaesth 1980;52:577583. 30. Lowenstein E, Foex P, Francis CM, et al. Regional ischemic ventricular dysfunction in myocardium supplied by a narrowed coronary artery with increasing halothane concentration in the dog. Anesthesiology 1981;55:349-359. 31. Francis CM, Foex P, Lowenstein E, et al. Interaction between regional myocardial ischaemia and left ventricular performance under halothane anaesthesia. Br J Anaesth 1982;54:965-980. 32. Cutfield GR, Francis CM, Foex P, et al. Myocardial function and critical constriction of the left anterior descending coronary artery: Effects of enflurane. Br J Anaesth 1980;52:953P.
33. Elzinga WE, Skinner DB. Hemodynamic characteristics of critical stenosis in canine coronary arteries. J Thorac Cardiovasc Surg 1975;69:217-222. 34. Hagl S, Heimisch W, Meisner H, et al. The effect of hemodilution on regional myocardial function in the presence of coronary stenosis. Basic Res Cardiol 1977;72:344-364. 35. Elliott PL, Schauble JF, Weiss J, et al. Echocardiography and LV function during anesthesia. Anesthesiology 1980;53:S105. 36. Reiz S, Balfors E, et al. Isoflurane: a powerful coronary vasodilator in patients with coronary artery disease. Anesthesiology 1983;59:91-97. 37. Reiz S, Balfors E, Gustavsson B, et al. Effects of halothane on coronary haemodynamics and myocardial metabolism in patients with ischemic heart disease and heart failure. Acta Anaesth Stand 1982;26:133-138. 38. Roy WL, Edelist G, Gilbert B. Myocardial ischemia during non-cardiac surgery procedures in patients with coronary artery disease. Anesthesiology 1979;51:393-397. 39. Prys-Roberts C, Greene LT, Meloche R, et al. Studies of anaesthesia in relation to hypertension: II. Haemodynamic consequences of induction and endotracheal intubation. Br J Anaesth 1971;43:531-547. 40. Giles RW, Berger HJ, Barash PG, et al. Continuous monitoring of left ventricular performance with the computerized nuclear probe during laryngoscopy and intubation before coronary artery bypass surgery. Am J Cardiol 1982;50:735-741. 41. Braunwald E, Kloner RA. The stunned myocardium-prolonged postischemic ventricular dysfunction. Circulation 1982;66:1146-1149.
245