An increased risk of perioperative cardiac arrest

in children, in comparison to adults, has been

recognized. A number of factors associated

with perioperative cardiac arrest have been identified,

including young age, comorbidities, and emergency

surgery. Since anesthesia-related cardiac arrest is

uncommon, a multi-related database is required to

understand the mechanisms of cardiac arrest and to

develop preventive strategies. Most cardiac arrests

occur during induction (37%) or maintenance (45%)

of anesthesia, usually following one or more of the

following antecedent events, i.e., bradycardia (54%),

hypotension (49%), abnormality of oxygen saturation

as measured by pulse oximetry (48%), inability to

measure blood pressure (25%), abnormality of endtidal

CO2 (21%), cyanosis (21%), or arrhythmia

(18%). In 11% of cases, cardiac arrest occurred

without recognized warning.1 There are only few

reports in the literature, and in Kariadi Hospital, none

has ever been reported. The aim of this report is to

identify and discuss possible causes of cardiac arrest

and to anticipate its complications

Prabakti, Yudhi

Siahaan, Edwin MP

Sidhartani,, M

Soemantri,, A

Soenarjo, Soenarjo

English

Diponegoro University Institutional Repository

132 • Paediatrica Indonesiana, Vol. 45 No. 5-6 • May - June 2005Paediatrica IndonesianaVOLUME 45 NUMBER 5-6May - June • 2005Case ReportFrom the Departments of Anesthesiology (S, YP, EMPS) and Child Health(AS, MS), Diponegoro University, Kariadi Hospital, Semarang.Reprint requests to: Yudhi Prabakti, MD, Department of Anesthesiology,Diponegoro University, Kariadi Hospital, Jl. Dr. Sutomo 16-18, Semarang5000. Tel./Fax. 62-24-8444346; E-mail: prabakti@yahoo.com.Cardiac arrest in a child during a combined generalepidural anesthesia procedureSoenarjo, MD, PhD; Yudhi Prabakti, MD; Edwin MP Siahaan, MD;A Soemantri, MD, PhD; M Sidhartani, MD, PhDsounds were normal. Everything was normal exceptfor a borderline hyperkalemia (K=5.1 mEq/l). Theanesthetic management consists of an inhalationinduction and atropine sulfate 0.02 mg/kg aspreanesthetic medication, with midazolam 0.1 mg/kgand ketamine 3 mg/kg, coadministered in one syringeintramuscularly before induction. As the patient wascalm, he was taken to the operating room forinduction of anesthesia.In the operating room, the patient was on elec-trocardiography (ECG), pulse oximetry, and auto-mated blood pressure monitor prior to anesthetic in-duction. Vital signs prior to induction showed a bloodpressure of 95/46 mmHg, heart rate (HR) of 98 beats/minute (bpm), and respiratory rate of 20 breaths/minute. Preoxygenation was initiated prior to induc-tion.Anesthesia was induced with the initial inhala-tion of 50% nitrous oxide and 50% oxygen at a totalflow of 6 l/minute. Halothane was introduced at 0.5%and was increased in 0.5% increments approximatelyevery three breaths. The induction progressedAn increased risk of perioperative cardiac arrestin children, in comparison to adults, has beenrecognized. A number of factors associatedwith perioperative cardiac arrest have been identified,including young age, comorbidities, and emergencysurgery. Since anesthesia-related cardiac arrest isuncommon, a multi-related database is required tounderstand the mechanisms of cardiac arrest and todevelop preventive strategies. Most cardiac arrestsoccur during induction (37%) or maintenance (45%)of anesthesia, usually following one or more of thefollowing antecedent events, i.e., bradycardia (54%),hypotension (49%), abnormality of oxygen saturationas measured by pulse oximetry (48%), inability tomeasure blood pressure (25%), abnormality of end-tidal CO2 (21%), cyanosis (21%), or arrhythmia(18%). In 11% of cases, cardiac arrest occurredwithout recognized warning.1 There are only fewreports in the literature, and in Kariadi Hospital, nonehas ever been reported. The aim of this report is toidentify and discuss possible causes of cardiac arrestand to anticipate its complications.Report of the caseA 4.5 year old, 14 kg boy was undergoing an electiveherniotomy to correct his  inguinal hernia. His medicalhistory was non-specific; vital signs were normal. Onphysical examination the lungs were clear and heartPaediatrica Indonesiana, Vol. 45, No. 5-6 • May - June 2005 • 133Soenarjo et al: Cardiac arrest during combined general epidural anesthesiasmoothly. The halothane vaporizer concentration hadreached 3.5% and was decreased to 2% upon intrave-nous (IV) catheter placement. The blood pressure wasthen 102/54 mmHg and the ECG revealed a normalsinus rhythm of 75 bpm. Atropine 0.02 mg/kg was ad-ministered intravenously. Heart rate increased to 145bpm. After using xylocaine spray on the oropharynx,tracheal intubation was facilitated by deepening theanesthesia. The trachea was intubated using a non-cuff Portex® endotracheal tube. After the breathsounds in both lungs were confirmed, the tube wasthen fixated and an oropharyngeal pack/mouth packwas inserted. While maintaining the anesthesia withspontaneous ventilation, we tried to initiate caudalblock for caudal analgesia in the left lateral position.While identifying the caudal epidural space using a23 gauge needle,  bradycardia with HR of 54 bpm andhypotension with BP of 62/45 mmHg occured. Soonoxygen saturation decreased until it was immeasur-able; so did the blood pressure. Heart rate wasaproximately 30-40 bpm. The patient then becamepulseless for about 2 minutes. As the bradycardia andhypotension occured, we abandoned the caudal blockattempt, turned the patient back to supine position,immediately administered atropine 0.5 mg IV, andperformed fluid challenge and resuscitation, with noresponse. Spontaneous ventilation was still present.Immediately after discovering that the patient waspulseless, we performed CPR with the patient in asupine, slightly head-down position. Adrenaline wasgiven every 3 minutes while continuing CPR, start-ing from 10 mg/kg (1:10,000)  and increased up to100 mg/kgBW (1:1000). We also gave defibrillatoryshocks of 25 joules, 25 joules, and 50 joule, consecu-tively, because a ventricular fibrillation ECG patternwas seen, followed again by adrenaline and CPR. Af-ter this, we gave three defibrillatory shocks of 50 joules,but the ECG showed an asystole pattern. After anhour of CPR, we stopped and decided to declare it asfailed resuscitation.DiscussionMedication-related problems are the most commoncause of cardiac arrest, accounting for 37% of all cases.Cardiovascular depression from the administration ofhalothane, halothane plus an intravenous medication(fentanyl, bupivacaine, lidocaine, propranolol,sufentanil, or thiopental), or sevoflurane was regardedas the primary cause in 71% of all medication-relatedcases. The median age for the 37 cardiac arrests relatedto halothane (either alone or in combination with anintravenous medication) was 8 months (range 5 days-7 years). These patients were in American Society ofAnesthesiologists (ASA) physical status 1-2 and 3-5(because of congenital heart disease); but had anunrecognized cardiomyopathy. The median halothaneconcentration was 2%; some patients received 3-3.9%,and others received 4% or more halothane just priorto arrest. Sixty-six percent of halothane-related arrestsoccurred during induction, and 34% occurred duringthe maintenance phase. The most common antecedentevents were bradycardia and hypotension andabnormality in oxygen saturation as measured by pulseoximetry. The most common associated factors wereassisted or controlled ventilation and difficultintravenous access requiring multiple attempts.Patients were successfully resuscitated and recoveredwithout permanent injury. Epinephrine alone, atropinealone, or epinephrine plus atropine were the drugtreatments usually associated with the return ofadequate circulation.1,2,3Arrests related to cardiovascular depression fromsevoflurane occurred during induction of anesthesiain ASA physical status 3 children, preceded by hy-potension and bradicardia. Some children weresuccessfuly resuscitated and survived without se-quelae.4,5In some cases, the associated factors contribut-ing to cardiovascular depression by halothane werethe use of assisted or controlled ventilation, whichaccelerated the rise of halothane concentration in theblood and myocardium or reduced the cardiac outputby impeding venous return. Similarly, difficulty in in-travenous access may have resulted in prolonged ex-posure to high concentrations of inspired halothane.Patients with significant underlying disease such ascongenital heart disease may tolerate poorly anychange in cardiac output caused by halothane-in-duced reductions in heart rate or myocardial contrac-tility.It remains unclear at this time whether the in-creasing popularity of sevoflurane as an inductionagent in children will have an impact on the numberof reports of cardiac arrest attributed to inhalationPaediatrica Indonesiana134 • Paediatrica Indonesiana, Vol. 45, No. 5-6 • May - June 2005agents. It has been reported that compared to hal-othane, sevofurane has less potential for producingbradycardia and myocardial depression. Because de-nominators are not available, the incidences for hal-othane and sevoflurane-related cardiac arrests can-not be calculated.Most cases of accidental intravascular injectionof local anesthetics occurred during attempts at cau-dal injection despite negative aspiration and absenceof response to a test dose. Incremental dosing of localanesthetic into the epidural space has been recom-mended over bolus injection to allow earlier detec-tion of intravascuiar injection, although this has notbeen studied systematically. Alternatively, use of lo-cal anesthetics with less myocardial toxicity than thatassociated with bupivacaine might be recom-mended.1,3,6Regional anesthesia and nerve blocks are nowused widely in children, mostly in conjunction withgeneral anaesthesia. They provide part of the anaes-thetic and significantly improve patient comfort in thepostoperative period. Many advances have been madesince Curwen in Durban, South Africa presented anarticle in 1930 on 99 caudal blocks in neonates. Heconcluded his article wondering if he had done some-thing worthwhile or was it a technique that would beregarded as ridiculous.In Melbourne, caudal block has been used regu-larly in children for 30 years. Adaptations from adultpractice, particularly epidurals with catheters, andmore recently spinals for premature infants, develop-ment of block techniques resulting from anatomicalstudies, and better understanding of the drugs usedand their safety through measurement of blood con-centrations, have led to improvements in clinical prac-tice.8,9Sudden cardiac arrest during anesthesia in ap-parently healthy children may occur in the absenceof anesthetic overdose due to various preexisting con-ditions that may not be readily clinically apparent.Arrhythmias during anesthesia induction may becaused by factors such as hypoxia, hypercarbia, andstimulation during inadequate anesthesia. When un-diagnosed congenital cardiac anomalies, such as mi-tral valve prolapse, are exacerbated by anesthetic in-duction, arrhythmias and cardiovascular collapse mayresult. Ventricular bigeminy, multifocal prematureventricular contractions, and ventricular tachycardiahave been reported during anesthesia in a pediatricpatient who was subsequently diagnosed with mitralvalve prolapse.1,2,10The association of ventricular arrhythmias withhalothane, hypercarbia, and atropine cannot be ig-nored in the present case. Ventricular extrasystolesare more common in children receiving intravenousatropine during halothane anesthesia with spontane-ous ventilation than in those who did not receive at-ropine. However, in a more recent study of intrave-nous atropine administration during halothane anes-thesia, no ventricular extrasystole was noted. In thisstudy, ventilation was often assisted or controlled. Ina study of cardiac arrhythmias in pediatric patients,there were significantly more ventricular arrhythmiasin children whose airways were managed with a maskthan in those managed by endotracheal intubation.Additionaly, there was a strong relationship betweenventricular arrhythmias and hypercarbia in  childrenwhose airways were managed using a face mask. Un-fortunately, the timing of the arrhythmias and the useor nonuse of atropine were not reported.1,10Cardiac arrest during anesthesia is usually pre-ceded by bradycardia. The most common causes ofarrest in infants and children are anesthetic overdoseand failure to ventilate and oxygenate.Non-ventricular fibrillation or tachycardiaProfound bradycardia or asystole is the most commondysrhythmia associated with cardiac arrest in infantsand children. Profound bradycardia should thereforebe treated in the same way as asystole. The treatmentconsists of an initial dose of adrenaline of 10 mg/kgIV or by the intraosseous route (or 10 times this dosevia a tracheal tube if venous access has not beenestablished). Recent studies in animals and childrenhave suggested the benefit of a higher dose ofadrenaline for the unresponsive asystolic child.Therefore, should the child not respond to the initialdose, another dose of 100 mg/kg is recommended.Further studies have shown that if the child does notrespond to this higher dose, the eventual outcome islikely to be poor.  In reviewing the results of thesestudies, no children survived to discharge of thosegiven more than two doses of adrenaline.When there is a cardiac rhythm but no cardiacoutput (electromechanical dissociation/pulseless elec-Paediatrica Indonesiana, Vol. 45, No. 5-6 • May - June 2005 • 135Soenarjo et al: Cardiac arrest during combined general epidural anesthesiatrical activity) it is also necessary to treat any of theunderlying reversible causes of the arrest. Hypoxia,hypovolemia, tension pneumothorax, cardiac tampon-ade, drug overdose, hypothermia, and electrolyte im-balance are all treatable, and resuscitation attemptsshould not be abandoned until a reasonable attempthas been made to correct these potentially reversiblecauses of cardiac arrest 4,5,7.Ventricular fibrillation and tachycardiaThese rhythms, although common in adults, arerelatively rare in infants and children. Although onestudy reported an incidence of ventricullar fibrillationof 23% in children, most other studies have reportedan incidence of 0-10%. Nonetheless, the physicianmust always be aware of the occasional need to treatventricular fibrillation in children by defibrillation.The recommended sequence is to give two rapiddefibrillatory shocks of 2 J/kg, followed by a singleshock at 4 J/kg. All further defibrillation attemptsshould then be made at 4 J/kg in a rapid repeated se-ries of three shocks. After the first cycle of threedefibrillation attempts, adrenaline 10 mg/kg shouldbe given and another dose of 100 mg/kg after the sec-ond cycle of three shocks and between all subsequentcycles. When ventricullar fibrilation occurs in chil-dren there is often an underlying cause and correc-tion of hypothermia, drug overdose (tricyclic antide-pressant overdose) and electrolyte imbalance (hyper-kalemia) should be considered 4,5,7.Halothane produces a dose-dependent reductionin cardiac output that principally reflects decreases instroke volume owing to reductions in myocardial con-tractility. Depression of myocardial contractility pro-duced by nitrous oxide is about one half that producedby a comparable concentration of a volatile anesthetic.As we know, the ability of volatile anesthetics to re-duce the dose of epinephrine necessary to evokeventricullar cardiac dysrhythmias in greatest withhalothane. Halothane also slows the rate of sinoatrialnode discharge and prolongs Purkinje fibre andventricullar conduction time. Indeed halothane hasnegative inotropic, vasodilating, and depressant effectson the sinoatrial node which are similar to the effectsproduced by calcium entry blockers 11.The cardiovascular effects of ketamine whenadministered in the presence of halothane may re-sults in hypotension. Halothane, by decreasing  therelease of norepinephrine, could direct allow the car-diac depressant effect of ketamine to manifest.Ketamine causes a dose-dependent decrease in hal-othane anaesthetic requirement (MAC). Halothaneprolongs the duration of action of ketamine by delay-ing redistribution and metabolism 12.The cardiotoxic effects of excessive potassiumor hyperkalemia are very important. Impaired excit-ability, automaticity, conductivity, and contractilitymay result. Signs and symptoms of increased serumpotassium are mental confusion, sense of weakness,and, most importantly, bradycardia and irregularrhythms, peripheral vascular collapse and hypoten-sion, muscular paralysis, and cardiac arrest 13.Since the attempt of caudal block had beenstopped at the time of identification of the caudalepidural space, we presumed that hypotension, brady-cardia, and cardiac arrest with ventricular fibrillationand ventricular tachycardia during CPR may be re-lated with medication and cardiovascular pathologyof undetermined etiology and hyperkalemia.ConclusionThe cardiotoxic effect of hyperkalemia and generalanesthesia may have caused the cardiac arrest in thiscase. Furthermore, the cardiodepressant effect ofketamine was augmented by halothane and nitrousoxide.References1. Morray JP, Geiduschek JM, Ramamoorthy C, HaberkernCM, Hackel A, Caplan RA, et al. Anesthesia-relatedcardiac arrest in children: Initial findings of the Pediat-ric Perioperative Cardiac Arrest (POCA) Registry. An-esthesiology 2000; 93:6-14.2. Moritz HA, Parnass SM, Mitchell JS. Ventricular fi-brillation during anesthetic induction in a child withundiagnosed mitral valve prolapse. Anesth Analg1997;85:59-61.3. Curatolo M, Scaramozzino P, Venuti FS, Orlando A,Zbinden AM. Factors associated with hypotension andbradycardia after epidural blockade. Anesth Analg1996;83:1033-40.Paediatrica Indonesiana136 • Paediatrica Indonesiana, Vol. 45, No. 5-6 • May - June 20054. Gabbott DA, Baskett PJF. Management of the airwayand ventilation during resuscitation. Br J Anaesth1997;79:159-71.5. Zideman DA. Pediatric and neonatal life support. Br JAnaesth 1997;79:178-87.6. Sprung J, Abdelmalak B, Schoenwald PK. Vasovagalcardiac arrest during the insertion of an epidural cath-eter and before the administration of epidural medica-tion. Anesth Analg 1998;86:1263-65.7. Zideman DA. Resuscitation. Br J Anaesth 1999; 83:157-68.8. Brown TCK, Eyres RL, McDougall RJ. Local and re-gional anesthesia in children. Br J Anaesth 1999;83:65-77.9. Roelants F, Veyckemans F, Van Obbergh L, Singelyn F,Waterloos H, Gribomont BF. Loss of resistance to sa-line with bubble of air to identify the epidural space ininfants and children. Anesth Analg 2000;90:59-61.10. Keats AS. The role of anesthesia in surgical mortality.In: Gravenstein N, editor. Complication in anesthesi-ology. 2nd ed. Philadelphia: Lippincott Raven; 1996.p. 27-36.11. Stoelting RK. Inhaled Anesthetics. In: Stoelting RK,editor. Pharmacology and physiology in anasthetic prac-tice. 2nd ed. Philadelphia: Lippincott Raven; 1991. p.33-69.12. Stoelting RK. Nonbarbiturate induction drugs. In:Stoelting RK, editor. Pharmacology and physiology inanasthetic practice. 2nd ed. Philadelphia: LippincottRaven; 1991. p. 134-47.13. Collins VJ. Fluids and electrolytes. In: Collins VJ, edi-tor. Physiology and pharmacology based of anesthe-sia. Philadelphia: Williams and Wilkins; 1996. p. 165-87.

Anesthesia-related cardiac arrest in children: Initial findings of the Pediatric Perioperative Cardiac Arrest (POCA) Registry. Anesthesiology

Factors associated with hypotension and bradycardia after epidural blockade.

Fluids and electrolytes.

Inhaled Anesthetics. In: Stoelting

Local and regional anesthesia in children.

Loss of resistance to saline with bubble of air to identify the epidural space in infants and children.

Management of the airway and ventilation during resuscitation.

Nonbarbiturate induction drugs. In:

Pediatric and neonatal life support.

The role of anesthesia in surgical mortality.

Vasovagal cardiac arrest during the insertion of an epidural catheter and before the administration of epidural medication.

Ventricular fibrillation during anesthetic induction in a child with undiagnosed mitral valve prolapse. Anesth Analg

Cardiac arrest in a child during a combined general

epidural anesthesia procedure

http://eprints.undip.ac.id/1160/1/45-5-6-8.pdf

Cardiac arrest in a child during a combined general epidural anesthesia procedure

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