Brugada syndrome - a review of the implications for the anaesthetist.
The association with malignant arrhythmias is of concern to the anaesthetist. Perioperative pharmacological and physiological changes may precipitate these events and cardiac dysfunction. As the condition is increasingly being recognised, so more patients are likely to present for anaesthesia for treatment of the syndrome by implantable cardiac defibrillator (ICD) insertion, or for non-related surgery.
Anaesthetists may be unfamiliar with the existence and implications of Brugada syndrome. Although the condition is rare, the implications are serious and may result in death. While there are many individual case reports, these represent a diverse range of anaesthetic management and recommendations. To our knowledge there has been no review of the evidence for anaesthesia in this condition. In this paper we critically appraise the available literature to identify any unifying features to determine whether any specific management can be recommended.
A search of multiple databases and online search engines was conducted using the term "Brugada syndrome" alone and in combination with "anaesthesia" or "anesthesia". We limited the search from February 1992 to 2011 and to articles written in the English language. This allowed us to identify papers useful for the clinical overview and those specific to anaesthesia in these patients. Articles obtained were reviewed for relevance and the reference lists checked for additional papers of interest.
OVERVIEW OF THE SYNDROME
Brugada syndrome is characterised by a distinctive ECG pattern of ST elevation in the right precordial leads in the absence of structural heart disease. Three repolarisation patterns are recognised (Figure 1). A definitive diagnosis (Type 1 abnormality) is made in the presence of coved ST segment elevation >2 mm in more than one right precordial lead (V1-3) followed by a negative T wave, and at least one clinical criterion from Table 1 (2). However, this definition may be modified as new evidence suggests a Type 1 ECG can be associated with sudden cardiac death even without additional clinical criteria (4). Other patterns (Type 2 and Type 3) that convert to a Type 1 ECG after sodium channel blockade can also be diagnostic in conjunction with clinical criteria (2).
[FIGURE 1 OMITTED]
The prevalence is quoted to be 5 in 10,000 people, although it is difficult to accurately estimate because concealed forms of the disease may increase the actual prevalence (5). Important ethnic and geographical differences exist. It is more widely reported in Asia than in Western Europe and North America (3). Australia is expected to have a prevalence somewhere between the two because of the high proportion of South East Asian immigrants (6). In South East Asia, the syndrome is thought to be endemic, where it is believed to cause four to 10 sudden deaths per 10,000 people per year (7). This makes it the most important cause of sudden death in young males and is labelled "sudden unexplained nocturnal death syndrome" (7). It is also considered to be one of the causes of sudden infant death syndrome.
Brugada syndrome is one of the "channelopathies". These are conditions produced by alterations in the transmembrane ion channels responsible for the cell action potential, and which increase susceptibility to arrhythmias (4). Autosomal dominant transmission is usual although sporadic cases are known to occur (3,5). Different phenotypes exist, with some individuals more severely affected than others. Men are clinically affected eight to 10 times more commonly than women (3).
Mutations of the SCN5A gene responsible for the alpha subunit of the cardiac sodium channel have been implicated in approximately 20 to 25% of individuals (3). Numerous mutations have been discovered and in most, there is demonstrable loss of the sodium channel current (8). However, genetic heterogeneity is suggested by the low incidence of SCN5A mutations in affected patients. Recent findings of calcium channel abnormalities in such patients suggest the syndrome may be secondary to an imbalance between the inflow and outflow currents during the cardiac action potential (4,5).
Studies have explored the cellular and molecular basis of the diagnostic ECG changes and the susceptibility for ventricular fibrillation and sudden death (5). Loss of sodium channel function leads to imbalance of currents during phase 1 of the cardiac action potential and a characteristic notch in regions of the epicardium but not endocardium. The resulting transmural voltage gradient produces the characteristic ST segment elevation (9). The right ventricular outflow tract is most susceptible to these ECG changes because there are more prominent transient outward currents in the right compared to left ventricular epicardial and mid-myocardial cells. The susceptibility to ventricular arrhythmias can be explained by the imbalance of currents creating a vulnerable window during which time an extrasystole can trigger a phase 2 re-entry arrhythmia (9). This imbalance between inward and outward currents also helps explain some of the features of the syndrome, the effects of different modulating agents and conditions which subsequently have been used to confirm diagnosis and to plan treatment (4).
Autonomic tone, in particular increased vagal tone relative to sympathetic tone, affects ion channel flux (4). Beta-adrenergic blockade and alpha-receptor agonists can aggravate the characteristic ST changes by exacerbating the ion current imbalances during the early part of the myocardial action potential (10). Parasympathetic stimulation can augment these changes (10). Temperature changes can accentuate premature inactivation of the sodium channel and unmask silent forms of the disease, increasing the risk of arrhythmias3. Various treatments and clinical states have been implicated in modulating, unmasking and inducing the Brugada ECG pattern. These include antiarrhythmic agents such as sodium and calcium channel blocking agents, beta blockers, nitrates, psychotropic drugs, cocaine and alcohol intoxication (4,11).
Clinical features and diagnosis
Most patients remain asymptomatic, but 17 to 42% of diagnosed individuals will present with either syncope at some time during their lives (5) or sudden cardiac death secondary to ventricular arrhythmia. Symptom onset is usually around the fourth decade, although the condition has been described in both paediatric and elderly populations (3). Syncope and paroxysmal palpitations are the only symptoms of the disease that may give any warning before (aborted) sudden arrhythmic death occurs (12). Around 20% of patients may suffer supraventricular arrhythmias, most commonly atrial fibrillation (13). Like other channelopathies, arrhythmias and symptoms typically occur at times of rest or sleep when vagal activity predominates.
Although a definitive diagnosis is made with a Type 1 ECG pattern, other clinical situations can result in a similar ECG pattern and should be excluded (e.g. atypical right bundle branch block, acute myocardial infarction, pericarditis, pulmonary embolus, early repolarisation syndrome and electrolyte disorders) (9). However, it is well recognised that the classical ECG pattern can be intermittent and is often concealed, making the diagnosis not always apparent3. Repetitive ECG testing on patients with an initial diagnostic ECG found that almost all had at least one non-diagnostic ECG over a median period of 12 days and almost one-third of patients with a non-diagnostic ECG went on to develop a type 1 ECG pattern over a median period of 16 days (14). Serial ECG recordings are therefore recommended in all patients. Placement of right precordial leads in an upper position (second or third intercostal spaces) can increase ECG sensitivity (5).
When concealed, the ECG changes can often be unmasked by administration of sodium channel blocking agents. This is the basis of diagnostic testing and the syndrome is confirmed if a type 1 ECG appears (2).
Risk stratification and treatment
Once diagnosed, the patient is stratified to identify those at high risk of sudden death. There is debate regarding how this is best achieved12. Asymptomatic individuals are perceived as having lower risk of adverse events compared to those with the spontaneous ECG patterns and history of syncope. To date, the only proven effective treatment remains an ICD4. Generally, symptomatic patients will receive an ICD but other therapeutic strategies, utilising pharmacological agents such as quinidine, are under review.
Screening of family members following a confirmed case of Brugada syndrome or sudden cardiac death is recommended. Serial ECGs and a pharmacological drug challenge can assist risk stratification. Similarly, patients who are found to have a spontaneous or suspicious Brugada like-ECG on routine screening require further investigation12 although the risk of serious arrhythmias in asymptomatic patients is not clear.
BRUGADA SYNDROME--IMPLICATIONS FOR THE ANAESTHETIST
Known patients may present to anaesthetists for insertion of an ICD or non-related surgery. Anaesthetists may also become involved with these patients in the emergency department. Brugada tachyarrhythmias can present with seizures and the clinical picture of cerebral hypoperfusion secondary to cardiac arrhythmia has been confused with a postictal state11,15. However, previously undiagnosed Brugada syndrome may present for the first time during surgery raising the suspicion that anaesthesia or surgery may precipitate events in otherwise asymptomatic individuals. The risk of ventricular arrhythmias in the perioperative period is of concern as the pharmacological and physiological changes that occur during anaesthesia are implicated in precipitating such events. An understanding of the modulating agents and conditions is essential to allow planning of appropriate techniques and crisis avoidance (15,16).
Data regarding anaesthesia for these patients are limited to individual case reports or case series including small numbers. Our search found 18 clinical reports of anaesthesia including a total of 28 patients (17-32). Most involved general anaesthesia alone, although three patients also had an epidural and one included a paravertebral block (16,20,28,29). There was only one spinal anaesthetic and one interscalene brachial plexus block (23,32). Two paediatric patients were reported (17,18). We critically appraise the literature and present the anaesthetist with clinically relevant information based on the limited available evidence.
An undiagnosed patient presenting with a suspicious ECG on routine testing in the peri-operative period should ideally undergo further cardiac evaluation prior to anaesthesia, especially if other clinical criteria are present (Table 1). Previously, a patient displaying a characteristic Type 1 ECG without additional clinical criteria would be classified as having an idiopathic Brugada ECG and not Brugada syndrome (5). More recently, it has been recommended that all patients with a type 1 ECG, even when isolated, should be considered at risk of sudden death4. It would seem sensible to treat these patients undergoing anaesthesia as having the condition. Those patients with an ICD in place should ideally have it turned off preoperatively to prevent monopolar diathermy causing inappropriate activation. External defibrillator pads should be applied and remain until the ICD can be reactivated after surgery.
Hyperkalaemia, hypokalaemia and hypercalcaemia can both unmask or modulate Brugada ST segment elevation and should be corrected preoperatively3. Sodium and calcium channel blockers, nitrates, tricyclic and tetracyclic antidepressants, phenothiazines, carbamazepine, phenytoin, selective serotonin reuptake inhibitors and lithium all produce similar effects and may increase the risk of adverse events11,33. Sedative premedication with the benzodiazepines has been used uneventfully (17,22,24,32).
Choice of regional vs general anaesthesia
There are few reports of regional techniques used as the primary anaesthetic technique. Anaesthetists may have chosen to avoid such techniques because of the theoretical risk of problems when using local anaesthetic drugs with sodium channel blocking properties.
Two of the three reported cases involving epidural anaesthesia reported problems (16,20). In both cases, there was no preoperative diagnosis of Brugada syndrome. One patient developed typical ECG changes and hypotension early in the postoperative period (16). The other developed a Brugada ECG and frequent ventricular extrasystoles that evolved into ventricular tachycardia and repetitive ventricular arrhythmias (electrical storm) (20). This patient subsequently received another epidural bupivacaine infusion for a second operation during the same admission that also resulted in Brugada ECG changes without cardiovascular compromise. In all cases, the changes completely resolved on discontinuation of the epidural bupivacaine infusion. An asymptomatic patient with an unrecognised preoperative Brugada ECG underwent general anaesthesia combined with a thoracic paravertebral block using 40 ml 0.5% ropivacaine (28). The patient developed intraoperative bradycardia, polymorphic ventricular tachycardia and hypotension requiring inotropic support shortly after surgery commenced. Symptoms resolved spontaneously.
An epidural bupivacaine infusion has been administered to a known Brugada syndrome patient without incident (29). However, the authors still advise caution administering local anaesthetics in areas where systemic absorption may be rapid. More recently, a symptomatic patient with an implanted ICD underwent an uneventful ultrasound-guided interscalene block using 40 ml of 1.5% mepivacaine for arthroscopic acromioplasty (32). Although this appears to be an unnecessarily high dose based on recent evidence (34,35), there were no adverse perioperative events. One report of spinal anaesthesia using 10 mg of 0.5% bupivacaine for repair of fractured patella was uneventful (23). We have used lignocaine uneventfully for ultrasound guided peripheral nerve blocks in a patient with a strong family history and syncope for K-wiring of metacarpal fractures (unpublished). There are two reports of local anaesthetic infiltration in known Brugada patients. A child received 1.25 mg/kg bupivacaine following an open right inguinal hernia repair (17) and an adult patient received 15 mg of lignocaine with adrenaline intraorally during maxillofacial surgery (27). Another two patients received lignocaine boluses intravenously to enhance cardio-stability at intubation when scheduled for ICD implantation (22). There were no arrhythmic consequences in any of these cases.
From the cases described, there is conflicting evidence regarding whether regional anaesthesia is safe. Most adverse events occurred in patients who had little or no reason to suspect the condition. This may support the suspicion that local anaesthetic drugs may unmask the disorder. Where local anaesthetics have been implicated in the development of Brugada ECG changes and cardiovascular instability, there has likely been rapid absorption into the systemic circulation, although serum levels have not been measured to confirm this. Peripheral nerve blocks may have potential advantages over general anaesthesia and central neuraxial blockade. They are less likely to induce sudden drug-related autonomic changes and reduce the risk of poor analgesia or light anaesthesia if performed accurately.
Techniques involving local anaesthetics should ideally incorporate strategies to reduce drug dose such as the use of ultrasound guidance. The local anaesthetic agent should be chosen carefully. Local anaesthetic agents with slow dissociation characteristics are more likely to unmask the Brugada phenotype and precipitate arrhythmias (36). Bupivacaine causes depression of the rapid phase of depolarisation and remains bound to sodium channels longer than other local anaesthetic agents and should be avoided in patients with Brugada syndrome (11). Although a recent case of lignocaine-induced Brugada ECG has been reported in a patient with a novel double mutation of the SCN5A gene (36), it is generally believed that lignocaine is safe if combined with adrenaline and used in low dose (11). Longer-lasting anaesthesia or analgesia could therefore be produced by lignocaine infusions or repeated bolusing through a continuous nerve catheter.
Induction and maintenance of anaesthesia
The choice of induction agent is probably not critical. Midazolam, propofol, barbiturates and fentanyl have all been used successfully on many occasions. However, propofol is listed as a drug to be avoided11. This recommendation is based mainly on adverse events which occurred during prolonged infusion causing propofol infusion syndrome. This is generally associated with infusions greater than 4 mg/kg/hour for more than 48 hours, although it has been observed within five hours (37). In some instances, sudden cardiac death has resulted after development of ST segment elevation similar to that seen in the Brugada ECG. In some patient groups, it is suggested that development of a Brugada-like ECG is a sign of cardiac electrical instability that may predict imminent cardiac death (20,38). Maintenance of anaesthesia with propofol has been used successfully (22,30) but should ideally use the lowest feasible doses for the shortest time possible. Ketamine can also precipitate characteristic Brugada ECG changes when taken in recreational overdose (39).
There is no evidence regarding the ideal volatile anaesthetic agent in Brugada syndrome. Isoflurane and sevoflurane have been used in air and nitrous oxide without incident. The association with SCN5A gene mutations in the long QT syndrome (40) has made some authors recommend using sevoflurane (15,17) as it has no effect on QT length, unlike halothane and isoflurane (41). Some advocate monitoring depth of anaesthesia to assist dose limitation (30).
In addition to standard monitoring, ST trend analysis (15,26) and 5-lead ECG monitoring have been suggested (15,21,24,26,30). Developing ST segment elevation may be a warning sign of impending electrical instability and immediate corrective measures are needed20. Invasive blood pressure monitoring and central venous access may be beneficial for major cases (22,23,29).
All patients, including those without an ICD, should have external defibrillator pads placed prior to induction of anaesthesia.
Autonomic changes can contribute to the development of tachyarrhythmia. Factors known to affect autonomic tone such as inadequate analgesia, light anaesthesia and postural changes should be minimised. Depth of anaesthesia should be balanced to minimise these effects (21), as bradycardia or increased vagal tone as a result of surgical stimulation have also been implicated in the development of Brugada ECG changes (25). Some advocate avoiding suxamethonium due to the risk of bradycardia (18), with some using prophylactic glycopyrrolate prior to intubation (17). Temperature changes, especially increases, can unmask the syndrome (3). The patient should be warmed or cooled as appropriate to maintain normothermia, with monitoring for all but the shortest of cases (15,17,26).
Drugs that block sodium channels such as procainamide and flecainide are contraindicated (23). Beta-adrenergic blockade and alpha-receptor stimulation (norepinephrine and methoxamine) can augment ST elevation in Brugada syndrome (10), whereas beta-adrenergic stimulation minimises such manifestations. Perioperative beta-blockade should be avoided. Ephedrine has been used to treat perioperative hypotension because of its dual action (22,27). The use of a low-dose dopamine infusion to maintain heart rate has been described (19). It is widely advocated to have an infusion of isoprenaline available in case intraoperative ST segment changes occur (15,17,19,21,22,24,27). Neostigmine can cause ST segment elevation and some authors suggest avoiding it (15,23). One patient developed pulmonary oedema after neostigmine administration, although this patient concurrently suffered laryngospasm and negative pressure effects were considered a more likely cause (15). Others have used it cautiously without incident (21,24,29). Administering anti-muscarinic treatment prior to incremental neostigmine dosing has been advocated (21).
Acute myocardial ischaemia involving the right ventricular outflow tract mimics the ST segment elevation similar to that in Brugada syndrome and it is suggested that those with the syndrome may be at higher risk for ischaemia-related sudden death (3). Care should be taken to minimise perioperative myocardial ischaemia, which should be treated promptly.
Any patient with an ICD should have it switched back on as soon as possible and before removing external defibrillator pads. Arrhythmias can occur postoperatively and a period of continuous ECG monitoring with ST analysis for up to 36 hours has been recommended (15,17,21,23-26). Attention to all modulating factors should continue during this time. Phenothiazines are relatively contraindicated11, (42) so alternative antiemetic therapy should be utilised17.
In summary, there is relatively little evidence to guide the anaesthetic management of patients with Brugada syndrome. We present recommendations following critical review of these cases and experimental studies. However, it should be remembered that these patients show large and conflicting variation in response to certain drugs and conditions. Application of external defibrillator pads is recommended. Maintenance of general anaesthesia with propofol, if necessary, is recommended for short cases only. Regional anaesthetic techniques, especially peripheral nerve blocks, may be considered using limited doses and local anaesthetic adjuncts. The local anaesthetic of choice is lignocaine. Neuroaxial blocks should be developed slowly to avoid fast onset of deep sympathetic blockade as autonomic changes can affect the syndrome as well. A useful resource for clinicians caring for patients with Brugada syndrome is the website www.brugadadrugs.org which gives recommendations regarding drug safety (11).
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S. M. CAREY *, G. HOCKING ([dagger]) * M.B., Ch.B., F.R.C.A., Anaesthetic Fellow.
Department of Anaesthesia, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia
([dagger]) M.B., Ch.B., D.A., D.M.C.C., F.R.C.A., F.A.N.Z.C.A., F.F.P.M.A.N.Z.C.A., Clinical Associate Professor, School of Medicine, The University of Western Australia and Specialist Anaesthetist, Sir Charles Gairdner Hospital.
Address for correspondence: Dr G. Hocking, email: firstname.lastname@example.org Accepted for publication on March 2, 2011.
Table 1 Clinical criteria included in the diagnosis of Brugada syndrome Documented ventricular fibrillation Polymorphic ventricular tachycardia Family history of sudden cardiac death at <45 years old Coved-type ECGs in family members Inducibility of VT with programmed electrical stimulation Syncope Nocturnal agonal respiration ECG=electrocardiogram, VT=ventricular tachycardia.
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|Author:||Carey, S.M.; Hocking, G.|
|Publication:||Anaesthesia and Intensive Care|
|Date:||Jul 1, 2011|
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