Diagnosis of postoperative arrhythmias following paediatric cardiac surgery.
Postoperative arrhythmias cause significant morbidity and are associated with a higher hospital mortality(2,3). Bradyarrhythmias are more frequent than tachyarrhythmias; supraventricular tachycardias occur more frequently than ventricular tachycardias in the paediatric setting(1,2,4,5). The inconsistencies in the techniques used for diagnosis and definitions used to describe arrhythmias lead to inconsistent reporting, diagnosis and management strategies in the postoperative patient(6). The aims of this review are:
1. To describe the aetiological factors which predispose the child with CHD to arrhythmias in the PICU.
2. To provide a practical classification of arrhythmia mechanisms for the bedside clinician in the PICU.
3. To provide a practical outline of the techniques for prompt diagnosis of the common arrhythmias for the bedside clinician in the PICU.
4. To provide specific examples and practical guidelines for diagnosing common arrhythmias in the PICU.
THE AETIOLOGY OF ARRHYTHMIAS IN THE POSTOPERATIVE CARDIAC SURGERY PATIENT
The electrical events of the cardiac cycle depend on specialised conduction tissue and intercellular electrical connectivity to optimise cardiac filling and output. The co-ordinated rhythmic contraction of the heart begins with spontaneous depolarisation of cells in the sinoatrial node due to diastolic depolarisation and calcium cycling(7,8). The electrical wavefront spreads from the sinoatrial node to the surrounding atrial myocardium, causing atrial contraction. The atrioventricular node (AVN) then serves as the electrical junction between the atria and the ventricles. The existence of internodal pathways has been debated(9,10). The AVN is intended to be the only electrical connection between atrial and ventricular myocardium. Accessory connections can exist which allow conduction to proceed antegradely, retrogradely or in both directions between atrium and ventricle. The specialised structure of the AVN allows for diastolic filling of the ventricles before the His-Purkinje system activates the ventricular myocardium. The conduction system is designed to provide optimal synchronised contraction of the atria prior to ventricular contraction, known as atrioventricular (AV) synchrony. As the atrial and ventricular cells become electrically activated, calcium influx prompts myocyte contraction. Repolarisation is an active process with restitution of the membrane potential in anticipation of the next electrical stimulus. Carefully regulated acid-base status, electrolytes and temperature are necessary to maintain normal cardiac electrical activity. Therefore, cardiac surgery can affect the heart either at a macroscopic level or at a cellular level to promote arrhythmias.
Mechanisms of arrhythmias
In the clinical setting, arrhythmias are classified, based on the patient status as 'unstable' or 'stable'. This informs of the urgency for therapy. Beyond this, a mechanistic classification allows for a better understanding of the relationship between the underlying substrate and the therapy. Despite the multitude of factors which can cause arrhythmias, the mechanism can be categorised as shown in Table 1.
Automaticity refers to the ability of cardiac cells to depolarise spontaneously. Under normal circumstances, the greatest automaticity is in the cells of the sinoatrial node, followed by the cells of the AVN. Re-entrant circuits require two pathways capable of conduction with unilateral conduction delay in one limb and an intervening conduction barrier (Figure 1). Re-entry may involve a macrore-entrant circuit, such as occurs with an accessory pathway. Alternately, re-entry can involve a microre-entrant circuit as might be seen around a small area of scarring(11). Examples of re-entrant tachycardias are listed in Table 1. A third mechanism of arrhythmias is triggered activity, seen more commonly in certain arrhythmia substrates such as long QT syndrome and digoxin toxicity(12-14).
[FIGURE 1 OMITTED]
Anatomical and surgical factors
In children with CHD, preoperative and intraoperative factors contribute to the development of postoperative rhythm disturbances. The underlying anatomy is an important predictor of postoperative arrhythmias. Several congenital heart defects are associated with arrhythmia substrates (Table 1) (11,15-22).
Chronic volume or pressure loading leads to chamber hypertrophy and fibrosis. This and previous palliative or corrective surgery may result in anatomic barriers to conduction and scarring. This sets up re-entrant areas around areas of diminished electrical activity, such as is seen in incisional tachycardias, where a circuit exists around the non-conducting scar (23-25).
During the conduct of surgery itself, bypass cannulation is near the sinus node, which may impair sinus node automaticity. Sinus node dysfunction can be seen acutely and chronically following open heart surgery (11,26). Many procedures for the correction of CHD involve the manipulation of tissues in the vicinity of the AVN (e.g. ventricular septal defects, AV septal defects, arterial switch). Normal AVN conduction may be affected by tissue trauma related oedema or by direct injury from suture lines (26). Junctional ectopic tachycardia (JET)--the most common tachycardia in the postoperative CHD patient--occurs when surgery in the vicinity of the AVN results in local changes that appear to enhance Automaticity (27,29).
Electrolytes and metabolic state
Disturbances of electrolytes are common following open-heart surgery and can affect rate, rhythm and automaticity (30,31). The most common abnormalities affect potassium, magnesium and acid-base balance. Frequent monitoring of electrolytes and blood gases is imperative. Preoperative diuresis can predispose to sodium, potassium and magnesium depletion. Postoperative renal impairment, bleeding, blood transfusion and diuretic requirements can aggravate these electrolyte imbalances. Potassium is important for maintaining a stable cell membrane potential. Hypokalaemia (<3 mmol/l) increases the cell membrane potential and is associated with delayed conduction causing atrial and ventricular ectopy, atrial tachycardia and AV block. Ventricular tachycardia and fibrillation are uncommon. Hyperkalaemia is associated with sinus arrest and PR interval changes, although AV block is uncommon (30,32). Hyperkalaemia accompanies oliguria or renal failure and rapid blood transfusion for postoperative bleeding. Severe bradycardia, idioventricular rhythms, ventricular arrhythmias and asystole are seen at higher serum levels (32,33). Magnesium has many important functions on the cell membrane. It is a critical cofactor for Na+-k+-ATPase, a key transporter in maintaining the cell membrane potential, a regulator of some cell membrane k+ channels and calcium antagonist. Hypomagnesaemia is often associated with hypokalaemia. Ventricular ectopy and ventricular fibrillation has been described(34). Magnesium supplementation to maintain a normal serum magnesium have been proposed as a therapy for JET (29). Hypermagnesaemia is uncommon unless iatrogenic but can be associated with delays in AV and intraventricular conduction.
Management of arterial pH is controversial. Metabolic acidosis resulting from hypoperfusion is best managed by treating the underlying cause and optimising oxygen delivery rather than prescribing bicarbonate. In situations where oxygen delivery is severely impaired and further incremental improvement requires time, some clinicians prescribe bicarbonate to correct the metabolic acidosis although the supportive evidence of its effect on long term outcome is lacking. Caution with bicarbonate use in the situation of low cardiac output is warranted to prevent severe hypokalaemia and associated ventricular arrhythmias. Although commonly prescribed for hyperkalaemia, there is little supportive evidence for its use in this situation (35).
Fever is common in the postoperative period and reflects the inflammatory state induced by cardiopulmonary bypass. Fever increases the endogenous catecholamines and can accelerate automatic tachycardias.
The spectrum of medications that can predispose patients to postoperative arrhythmias is extensive. The most frequent medications prescribed in children with heart disease are diuretics. Diuretics commonly cause both acute extracellular and chronic intracellular electrolyte abnormalities and set the stage for arrhythmias. Drug interactions with antiarrhythmic agents in combination with electrolyte disorders are of particular importance. Atrioventricular block is the most common sideeffect of these agents in the postoperative period (36,37). Amiodarone is the most common antiarrhythmic used in postoperative paediatric cardiac intensive care (38). It is safe and effective but has interactions with a variety of medications; specifically amiodarone can lead to decreased clearance of digoxin resulting in toxicity (and atrioventricular block). In addition, all antiarrhythmic agents have the propensity to cause arrhythmias (proarrhythmia) due to direct or indirect effects on membrane ion conductance, which in turn alters the cardiac action potential.
Other medication-induced mechanisms of postoperative arrhythmia include QT prolongation, a disorder of prolonged ventricular repolarisation which needs to be recognised in the acute postoperative setting (www.qtdrugs.org). The more common medications which can prolong the QT interval include antiarrhythmic medications, macrolide antibiotics and antifungals. Calcium influx into cells is also a common pathway in the genesis of arrhythmias, particularly in automatic arrhythmias and those caused by triggered activity (30,31,39). Exogenous inotropes (catecholamines, phosphodiesterase inhibitors) are associated with an increase in arrhythmogenesis, presumably through their actions in increasing intracellular calcium. Dopamine in particular has been associated with JET(40). Beta-blockers can also be implicated if abruptly withdrawn preoperatively, leading to a postoperative sinus tachycardia and hypertension; postoperative use such as in coarctation repair may be associated with with bradycardia or AV block; or proarrhythmia.
IMPACT OF ARRHYTHMIAS IN THE POSTOPERATIVE SETTING
The common reasons for haemodynamic compromise with any arrhythmia in the child are related to rate (either too slow or too fast) and loss of AV synchrony (30). Cardiac output is determined by the stroke volume and the heart rate. Blood pressure is determined by the systemic vascular resistance and the cardiac output. In children, the primary way to increase cardiac output is to increase the heart rate. Therefore, arrhythmias which result in a low heart rate often lead to low cardiac output. Tachycardia can cause haemodynamic compromise by decreasing diastolic filling time and stroke volume, increasing myocardial oxygen consumption and impairing coronary perfusion. Blood pressure is maintained in both cases by increasing the systemic vascular resistance and therefore afterload.
Loss of AV synchrony also reduces cardiac filling. In a compliant heart, most of the ventricular filling occurs during the rapid early filling phase of ventricular diastole. Preoperative pressure and volume loading increase the role that atrial contraction plays in ventricular filling and cardiac output. While the preoperative anatomy may contribute to ventricular hypertrophy, thereby impairing diastolic compliance, cardiac surgery exacerbates this by increasing myocardial oedema and dysfunction. An increase in heart rate postoperatively results in a corresponding decrease in filling time. Therefore, in the acute postoperative period, atrioventricular synchrony plays a much greater role than in the same child preoperatively. Fortunately, most arrhythmias encountered in the postoperative period are transient in nature (41,42). As well, the effects of cardiopulmonary bypass are self-limited and the need for AV synchrony and chronotropic competence decrease as the child improves. The most common sustained arrhythmias are bradycardic: usually sinus node dysfunction or complete heart block. (1,5) These sometimes necessitate long-term pacemaker therapy. (43)
CLINICAL APPROACH TO THE DIAGNOSIS OF AN ARRHYTHMIA
The first priority in the child with a postoperative arrhythmia is ensuring that haemodynamic stability is established. The 2005 Pediatric Advanced Life Support algorithms are a useful approach to the initial management of arrhythmias in a child. (44) Accurate diagnosis and management of postoperative arrhythmias requires careful preoperative preparation and a team approach to care. A thorough understanding of the patient's anatomy and haemodynamics is essential.
On arrival in the PICU following cardiac surgery, the stability of the patient's underlying rhythm and dependence upon pacemaker function is important handover information between the cardiac anaesthetist and PICU physician. A systematic approach to monitoring and diagnosis of rhythm abnormalities includes a rhythm strip printout and a 12-lead electrocardiogram to establish a template to compare QRS morphology if an arrhythmia develops, or make a diagnosis of an existing arrhythmia. The latest generation of patient monitors is capable of multichannel recording and retrospective full disclosure review of all electrocardiographic data and events.
Simultaneously observing the arterial pressure and waveform looking for beat-to-beat variability in the pulse pressure can aid in detecting arrhythmias and pulsus paradoxus. A regular, biphasic atrial pulse contour on the bedside monitor is suggestive of AV synchrony, whereas a monophasic pulse contour, marked irregularity or the presence of atrial cannon waves provides evidence for a lack of appropriate AV synchrony. This lack of synchrony may be due to AV dissociation, retrograde activation of atria or normal activation in the presence of extreme first-degree AV block. An echocardiogram should be urgently obtained in any postoperative patient with new onset arrhythmia to exclude a haemodynamic cause, such as residual outflow tract obstruction, tamponade due to blood or myocardial swelling or reduced function. Compromise of coronary perfusion, such as can be seen in arterial switch operations, in the retrogradely perfused coronaries post-Norwood palliation for hypoplastic left heart syndrome or any other procedure involving coronary manipulation (e.g. Ross procedure) can lead to sinus tachycardia changes or bradycardia due to compromise of coronary perfusion.
In the presence of atrial pacing leads, accurate diagnostic information can be obtained by obtaining a multi-lead atrial electrogram recording. The atrial electrogram allows for precise identification of the timing of atrial depolarisation in relation to the ventricular QRS complex. An atrial electrogram can be recorded using standard electrocardiogram (ECG) equipment in one of two ways. A unipolar atrial recording is obtained by connecting the limbs as usual and the atrial wires to two of the precordial leads (e.g. V1 and V2) and simultaneously recording concurrent limb leads on the ECG (Figure 2A). If this does not yield a clear atrial electrogram, a bipolar atrial recording can be obtained by attaching the lower limb leads in the usual fashion and connecting the atrial epicardial wires to the right and left upper limb leads (Figure 2B). This generates a bipolar atrial electrogram in lead I and a 'hybrid' in leads II and III. This method has the disadvantage that concurrent surface limb leads are not available for simultaneous comparison. The resolution of atrial timing using either techniques of atrial electrocardiography is superior to that provided by the standard surface electrocardiogram.
In the case where atrial wires are not available, an oesophageal lead can be used to facilitate identifying the atrial depolarisation on the ECG. The oesophageal lead is passed through the nose or the mouth and positioned near the mid-oesophagus directly behind the left atrium. For the neonate or infant, optimal electrical signals are typically found at an insertion depth of 12 to 17 cm measured from the distal electrode to the nares or mouth. (45) The oesophageal probe can be connected to the ECG machine in the same way that the atrial epicardial wires can be, allowing a recording of the atrial electrogram.
The relationship between the atrial activity and the ventricular activity may be difficult to ascertain in some cases of tachycardia. Adenosine administered during the recording of an atrial electrogram can be diagnostic by transiently blocking AVN conduction. It is important to be able to pace and cardiovert in this situation, as adenosine may result in atrial arrhythmias, in addition to the anticipated bradycardia. (46)
Additional diagnostic information can be provided in patients with a tachycardia of unclear mechanism by a brief period of atrial overdrive capture that is abruptly terminated while observing the response. If the tachycardia is utilising a re-entrant circuit and the circuit can be penetrated by the external pacing stimuli, the tachycardia may terminate. If the tachycardia is automatic, it may be briefly suppressed before resuming. The role of overdrive pacing is discussed in detail elsewhere. (47)
SPECIFIC ARRHYTHMIA EXAMPLES
The arrhythmias most commonly encountered in the postoperative CHD patient are sinus bradycardia (relative or absolute), complete AV block and JET. However, for completeness, other less common arrhythmias are also described below. Figure 3 provides a practical approach to the accurate diagnosis of postoperative arrhythmias.
[FIGURE 2 OMITTED]
[FIGURE 3 OMITTED]
Sinus bradycardia (Figure 4A) is diagnosed on the surface ECG or atrial electrogram as a P wave preceding a normal QRS complex at a rate that is slow for age and physiologic requirements. The threshold for diagnosing sinus bradycardia is dependent on the age of the patient and the clinical circumstances. A wide range of heart rate definitions have been given, some referring to sleeping rates from 24 hour Holter studies, and others to the lower rates from an awake, standard ECG. For example, a heart rate of 65 beats/minute in a sleeping, sedated three-year-old with normal haemodynamics is within normal; whereas if the child were agitated or unstable and on inotropic support, a rate of 90 beats/minute would indicate a relative bradycardia. Due to the difficulty in defining sinus bradycardia, the prevalence of sinus bradycardia is frequently not reported; however, in one study(5) sinus bradycardia occurred in 46% of patients with arrhythmias. Whenever the ventricular rate appears to be lower than anticipated in a postoperative patient, it is important to exclude atrial tachycardias with 2:1 AV block, in which alternate P waves may be difficult to identify.
AV block is present when there is an abnormality of impulse propagation from atrium to ventricle. First-degree AV block (Figure 4B) is defined as a long conduction time from the onset of atrial depolarisation to ventricular depolarisation. This includes the trans-atrial conduction time and the AV nodal conduction delay. This is manifest as a P wave followed by a long PR interval before the QRS complex. The normal values are based on age and rate. (48) For example, a PR interval of 170 ms in a teenager is normal, but not if the heart rate is 150 beats/minute. In severe cases, the long conduction time from atrium to ventricle may impede ventricular filling as atrial depolarisation occurs prior to ventricular relaxation. First-degree AV block is common in the presence of CHD and in children with electrolyte disturbances or receiving antiarrhythmics.
There are two types of second-degree AV block. The first is known as Mobitz Type I or Wenckebach and typically reflects conduction delay at the AVN. This is manifest by progressive lengthening of the PR interval, with eventual non-conduction of a P wave (Figure 4C). Type II second-degree block is usually representative of a more advanced conduction abnormality of the His-Purkinje system. This is manifest by a constant PR interval with one or more P waves not conducting to the ventricle (Figure 4D). Second-degree block can result in inappropriately low ventricular heart rates. From published reports, the prevalence of second-degree AV block appears to be low in the postoperative period42. Second-degree block is a common cause of an irregular rhythm.
[FIGURE 4 OMITTED]
Third-degree AV block or complete heart block is present when impulses from the atrium are not conducted to the ventricles (Figure 4E). This is not synonymous with AV dissociation, which simply means that the atria and the ventricles are being driven by different pacemaking foci. For example, during JET with AV dissociation, the ventricle is being driven by a nodal focus, while the atria are driven by the sinus node. An appropriately timed sinus impulse can still be transmitted to the ventricles. Complete heart block is the most common postoperative arrhythmia requiring longterm therapy, and most commonly arises after surgery near the AV node (e.g. ventricular septal defect repair, atrioventricular septal defect repair, Tetralogy of Fallot repair). (49) The escape pacemaker can be AV nodal, from the His-Purkinje system, or ventricular, and the rate is usually too slow to maintain an adequate cardiac output in the postoperative setting. Without pacing, cardiac output is impaired by low heart rates and loss of AV synchrony. Spontaneous resolution is frequent and may occur in up to two-thirds of patients by nine days postoperatively. (50) Late recurrence has been reported in as many as 5% of transient cases (43) and late recovery may occur in as many as 10% of patients who receive pacemakers. (51) It is important to document even transient complete heart block, as it has been reported to be a predictor of mortality in certain groups. (3-5)
[FIGURE 5 OMITTED]
Tachycardias comprise the most difficult arrhythmia to accurately diagnose and treat in the postoperative period. The most common tachyarrhythmias in the postoperative period result from enhanced automaticity. These include sinus tachycardia, JET and ectopic atrial tachycardia (EAT). (39,52) The ECG and clinical features that would suggest enhanced automaticity as the cause of tachycardia include:
* onset with steady warming-up (increase) of the rate (over 10 to 20 cardiac cycles),
* termination with cooling-down (slowing) of the rate,
* a variable rate that changes with manipulation of autonomic tone or temperature,
* refractoriness to electrical cardioversion or overdrive pacing manoeuvres (although they may be transiently suppressed with overdrive pacing).
Sinus tachycardia (Figure 5A) is the most common form of tachycardia and can be difficult to diagnose, particularly when there is an associated first-degree AV block. In the absence of an associated first-degree AV block, the P wave is followed closely by a QRS, in a 1:1 relationship. The P wave morphology should be the same as the preoperative ECG, with a P wave axis consistent with origin at the superior vena cava-right atrial junction. The rate should be physiologic and does not usually exceed 220 beats/minute. In sinus tachycardia with first-degree block, the P wave may fall within the T wave and not be detected on surface ECG or be mistaken for a retrograde P wave. The wire study will demonstrate regular 1:1 relationship of the atrial impulse to the QRS with a relatively long PR interval for age and/or rate. Pacing at a rate just above the prevailing sinus rate should maintain 1:1 conduction, the same QRS morphology and PR interval. Sinus tachycardia also demonstrates a gradual warming-up and cooling-down to stimuli such as fever. A decrease in heart rate with optimising haemodynamics, controlling body temperature and providing adequate analgesia suggests an automatic focus, most commonly sinus tachycardia.
Postoperative JET (Figure 5B) is the most common postoperative malignant tachyarrhythmia and is caused by a focus of increased automaticity in the AV node or His bundle. (39,53) The morphology of the QRS complexes is usually the same as in normal sinus rhythm--either narrow complex or exhibiting pre-existent bundle branch block. The rhythm is usually incessant and, in cases with ventriculoatrial (VA) dissociation, the diagnosis is readily made (Figure 5C). The comparison to the sinus QRS is essential to exclude ventricular tachycardia (VT), particularly if the QRS is wide. It is not necessary to document VA dissociation as 1:1 retrograde conduction is well described, broadening the differential diagnosis to include sinus tachycardia with first-degree AV block or other tachycardias. The wire study can be used to exclude sinus tachycardia with first-degree block by careful comparison of RP and PR intervals during atrial and/or ventricular pacing (Figure 6). We recommend starting with atrial pacing and comparing the PR intervals between the intrinsic rhythm and the paced rhythm. Occasionally, ventricular pacing is diagnostic. For example, if the RP interval is significantly shorter during ventricular pacing than during tachycardia, the P wave is not likely to be retrograde and the diagnosis is likely to be sinus or ectopic atrial tachycardia. Pacing manoeuvres do not usually terminate JET; other forms of supra-ventricular tachycardia (SVT) should be considered if this occurs.
As with other tachycardias, haemodynamic compromise attributable to JET is due to the increased heart rate and loss of AV synchrony with resultant decreased cardiac output. Accelerated junctional rhythm can be thought of as 'slow JET' and should be watched closely as it may gradually, or suddenly, increase in rate and become clinically significant.
EAT (Figure 5D) may be either paroxysmal or incessant. The characteristic feature of EAT is an inappropriately elevated atrial rate with a brief warming-up and cooling-down. (15) The QRS during EAT should be the same as during sinus rhythm, unless there is aberrancy. Most patients demonstrate first-degree AV block while a small proportion have second-degree block. EAT is often refractory to medical therapy and is not usually responsive to direct current cardioversion, but may be briefly suppressed by pacing at a faster rate. Diagnosis is determined by demonstrating an elevated atrial rate, occasionally with a non-sinus P wave axis or morphology. The wire study would show a rapid atrial rate with 1:1 conduction and first-degree block or an atrial rate in excess of the ventricular rate, when there is associated second-degree block. The most important role of the wire study is to differentiate EAT from atrial flutter with a P wave buried in the QRS or T wave. This is important because flutter usually responds to overdrive pacing or cardioversion.
[FIGURE 6 OMITTED]
In contrast to automatic arrhythmias, the ECG and clinical features that would suggest re-entrant tachycardia include:
* abrupt onset and offset,
* abrupt termination with electrical cardioversion or overdrive burst pacing,
* ability to initiate and terminate with appropriately timed extra stimuli,
* minimal beat-to-beat variation.
Atrial flutter or intra-atrial re-entrant tachycardia can be seen in patients with CHD acutely and chronically. The latter refers to a tachycardia due to a macro re-entrant circuit which is distinct from the typical flutter circuit seen in the absence of structural heart disease. Intra-atrial re-entrant tachycardia can occur around incision sites from cannulation from bypass or around other barriers to conduction. Therefore, every patient undergoing open heart surgery has the potential substrate for intra-atrial re-entrant tachycardia. Due to rapid atrial rates, it is important to 'look for the missing P wave' in any patient with an unexplained persistent tachycardia (Figure 5E).
In patients with accessory pathways or dual AVN physiology, one can see re-entrant tachycardias in the postoperative period. The QRS during these forms of SVT should be the same as during sinus rhythm, unless there is aberrancy. An atrial electrogram during AV reciprocating tachycardia and AVN re-entrant tachycardia demonstrates a regular relationship of the atrial impulse with the QRS and a short RP interval. When a long RP interval (RP interval greater than PR interval) is observed, EAT and permanent junctional reciprocating tachycardia should be considered. Permanent junctional reciprocating tachycardia is an uncommon form of tachycardia but is due to a slowly conducting accessory pathway, resulting in a long RP interval, making the differentiation from EAT challenging(1,2,4) (Figure 5D). Overall, SVT, other than sinus tachycardia and JET, has a low prevalence and occurs in less than 5% of postoperative patients and accounts for less than 20% of the arrhythmias documented. (1,2,4,5)
The administration of adenosine induces block in the circuit, usually within the AV node. Termination of an arrhythmia by adenosine is essentially diagnostic of a re-entrant arrhythmia that uses the AV node as an essential part of the circuit (AVN reentrant tachycardia, AV reciprocating tachycardia). A rare exception is the occasional adenosine sensitive atrial 'ectopic' tachycardia or ventricular tachycardia. (46)
Ventricular tachycardia is an uncommon arrhythmia in children postoperatively, and occurs less than 2% of the time(53). It is important to bear in mind that in the PICU, VT can look relatively narrow (QRS ~100 ms) due to patient age, origin of the focus near the His-Purkinje system or rapidity of conduction. Asymptomatic premature ventricular contractions are not infrequent and have been seen in as many as 11% of all postoperative patients. (1-4) ECG criteria for diagnosis of VT include:
* AV dissociation (present in the majority of VT)--the absence of VA dissociation is not helpful, because VT may happen with 1:1 VA conduction.
* widened or change in morphology of QRS complex from baseline. The QRS complex in neonates and infants may appear to be relatively narrow but of different morphology compared with sinus.
* intermittent fusion or capture beats.
* narrowing of QRS during atrial pacing at a faster rate.
In the presence of surgically-induced bundle branch block, it can be difficult to distinguish VT from SVT in children. A wide QRS can also be due to aberrancy, medication effect, pre-existing conduction abnormalities, an antegrade conducting accessory pathway or a paced rhythm with tracking of a supraventricular arrhythmia. Distinguishing VT from SVT is clearly critical and, importantly, the rate and stability of the patient are not helpful in differentiating SVT with a wide QRS from VT in children. If the patient is stable, different manoeuvres can be used in an attempt to accurately diagnose the tachyarrhythmia. These include accurate recording of atrial electrograms and response to vagal manoeuvres or adenosine. Atrial pacing resulting in a narrowing of the QRS complex is suggestive that the arrhythmia is VT. In the unstable patient in whom the mechanism remains unclear, Pediatric Advanced Life Support guidelines should be followed and treatment for VT should be given. (44)
PREVENTION OF ARRHYTHMIAS
Earlier repair may reduce the effects of longstanding volume and pressure load, and late onset arrhythmias. For the critical care physician caring for children in the immediate post cardiac surgery period, the key to preventing postoperative arrhythmias is anticipation. This requires a thorough understanding of the preoperative anatomy and conduct of cardiopulmonary bypass, the surgical repair and surgical factors contributing to arrhythmias, and postoperative factors that exacerbate or cause arrhythmias. Most children with open heart surgery will return to the PICU with atrial and ventricular pacing wires. These wires should be attached to the temporary pacemaker and the pacemaker function checked. Fever exacerbates automatic foci so maintenance of normothermia is imperative. Inotropes should be continuously reassessed and minimised. Optimising lung recruitment and careful monitoring of arterial blood gases to minimise pulmonary vascular resistance is critical to prevent pulmonary hypertension and right atrial and ventricular distension. Maintaining normal electrolytes is most safely managed with set nursing orders for prescribing replacement doses of potassium or magnesium. In the setting of reduced renal function, early institution of peritoneal dialysis will prevent hyperkalaemia and hypermagnesaemia.
Abnormalities in cardiac rhythm are common following surgery for congenital heart disease and are an important cause of impaired cardiac output in this setting. Timely and accurate identification of the rhythm disturbance is mandatory, and allows for the institution of effective, rhythm-specific management strategies in these patients.
(1.) Hoffman TM, Wernovsky G, Wieand TS, Cohen MI, Jennings AC, Vetter VL et al. The incidence of arrhythmias in a pediatric cardiac intensive care unit. Pediatr Cardiol 2002; 23:598604.
(2.) Pfammatter JP, Bachmann DC, Wagner BP, Pavlovic M, Berdat P, Carrel T. Early postoperative arrhythmias after open-heart procedures in children with congenital heart disease. Pediatr Crit Care Med 2001; 2:217-222.
(3.) Rekawek J, Kansy A, Miszczak-Knecht M, Manowska M, Bieganowska K, Brzezinska-Paszke M et al. Risk factors for cardiac arrhythmias in children with congenital heart disease after surgical intervention in the early postoperative period. J Thorac Cardiovasc Surg 2007; 133:900-904.
(4.) Delaney JW, Moltedo JM, Dziura JD, Kopf GS, Snyder CS. Early postoperative arrhythmias after pediatric cardiac surgery. J Thorac Cardiovasc Surg 2006; 131:1296-1300.
(5.) Valsangiacomo E, Schmid ER, Schupbach RW, Schmidlin D, Molinari L, Waldvogel k. Early postoperative arrhythmias after cardiac operation in children. Ann Thorac Surg 2002; 74:792-796.
(6.) Gengsakul A, Potts JE, Sandhu A, Patterson MWH, Sett SS, Taylor G. Documenting junctional ectopic tachycardia following pediatric open heart surgery. J Med Assoc Thai 2005; 88 (Suppl 3):S214-222.
(7.) Wetzel GT, Klitzner TS. Developmental cardiac electrophysiology recent advances in cellular physiology. Cardiovasc Res 1996; 31:E52-60.
(8.) Maltsev VA, Lakatta EG. Dynamic interactions of an intracellular Ca2+ clock and membrane ion channel clock underlie robust initiation and regulation of cardiac pacemaker function. Cardiovasc Res 2008; 77:274-284.
(9.) Anderson RH, Yanni J, Boyett MR, Chandler NJ, Dobrzynski H. The anatomy of the cardiac conduction system. Clin Anat 2009; 22:99-113.
(10.) James TN. The internodal pathways of the human heart. Prog Cardiovasc Dis 2001; 43:495-535.
(11.) Balaji S, Harris L. Atrial arrhythmias in congenital heart disease. Cardiol Clin 2002; 20:459-468, vii.
(12.) Bayer MJ. Recognition and management of digitalis intoxication: implications for emergency medicine. Am J Emerg Med 1991; 9:29-32; discussion 33-34.
(13.) Garson A Jr, Dick M 2nd, Fournier A, Gillette PC, Hamilton R, Kugler JD et al. The long QT syndrome in children. An international study of 287 patients. Circulation 1993; 87:18661872.
(14.) el-Sherif N. Early afterdepolarizations and arrhythmogenesis. Experimental and clinical aspects. Arch Mal Coeur Vaiss 1991; 84:227-234.
(15.) Triedman JK, Jenkins KJ, Colan SD, Saul JP, Walsh EP. Intraatrial reentrant tachycardia after palliation of congenital heart disease: characterization of multiple macroreentrant circuits using fluoroscopically based three-dimensional endocardial mapping. J Cardiovasc Electrophysiol 1997; 8:259-270.
(16.) Balaji S, Lau YR, Case CL, Gillette PC. QRS prolongation is associated with inducible ventricular tachycardia after repair of tetralogy of Fallot. Am J Cardiol 1997; 80:160-163.
(17.) Mandapati R, Walsh EP, Triedman Jk. Pericaval and periannular intra-atrial reentrant tachycardias in patients with congenital heart disease. J Cardiovasc Electrophysiol 2003; 14:119-125.
(18.) Tada H, Nogami A, Naito S, Suguta M, Hoshizaki H, Oshima S et al. Selected slow pathway ablation in a patient with corrected transposition of the great arteries and atrioventricular nodal reentrant tachycardia. J Cardiovasc Electrophysiol 1998; 9:436-440.
(19.) Pfammatter J-P, Wagner B, Berdat P, Bachmann DCG, Pavlovic M, Pfenninger J et al. Procedural factors associated with early postoperative arrhythmias after repair of congenital heart defects. J Thorac Cardiovasc Surg 2002; 123:258-262.
(20.) Bae E-J, Noh C-I, Choi J-Y, Yun Y-S, kim W-H, Lee J-R et al. Twin AV node and induced supraventricular tachycardia in Fontan palliation patients. Pacing Clin Electrophysiol 2005; 28:126-134.
(21.) Cheung YF, Cheng VY, Yung TC, Chau Ak. Cardiac rhythm and symptomatic arrhythmia in right atrial isomerism. Am Heart J 2002; 144:159-164.
(22.) knott-Craig CJ, Goldberg SP, Overholt ED, Colvin EV, Kirklin Jr. Repair of neonates and young infants with Ebstein's anomaly and related disorders. Ann Thorac Surg 2007; 84:587-592; discussion 592-593.
(23.) kurer CC, Tanner CS, Vetter VL. Electrophysiologic findings after Fontan repair of functional single ventricle. J Am Coll Cardiol 1991; 17:174-181.
(24.) Nurnberg JH, Ovroutski S, Alexi-Meskishvili V, Ewert P, Hetzer R, Lange PE. New onset arrhythmias after the extracardiac conduit Fontan operation compared with the intraatrial lateral tunnel procedure: early and midterm results. Ann Thorac Surg 2004; 78:1979-1988; discussion 1988.
(25.) Anderson RH, Ho SY. The morphologic substrates for pediatric arrhythmias. Cardiology in the Young 1991; 1:159-176.
(26.) Dodge-khatami A, Miller OI, Anderson RH, Goldman AP, Gil-Jaurena JM, Elliott MJ et al. Surgical substrates of postoperative junctional ectopic tachycardia in congenital heart defects. J Thorac Cardiovasc Surg 2002; 123:624-630.
(27.) Polderman kH, Girbes AR. Severe electrolyte disorders following cardiac surgery: a prospective controlled observational study. Crit Care 2004; 8:R459-466.
(28.) Lan Y-T, Lee JCR, Wetzel G. Postoperative arrhythmia. Curr Opin Cardiol 2003; 18:73-78.
(29.) Dorman BH, Sade RM, Burnette JS, Wiles HB, Pinosky ML, Reeves ST et al. Magnesium supplementation in the prevention of arrhythmias in pediatric patients undergoing surgery for congenital heart defects. Am Heart J 2000; 139:522-528.
(30.) Chung Ek. Electrolyte imbalance and cardiac arrhythmias. In: Principles of cardiac arrhythmias. Baltimore, Md. Williams & Wilkins 1983.
(31.) Zipes DP, Jalife J, Consult LLC. Ventricular tachycardia versus Supraventricular tachycardia with aberration In: Cardiac electrophysiology from cell to bedside. Philadelphia, Pennsylvania: WB Saunders Company 2000.
(32.) Woodforth IJ. Resuscitation from transfusion-associated hyperkalaemic ventricular fibrillation. Anaesth Intensive Care 2007; 35:110-113.
(33.) Alfonzo AVM, Isles C, Geddes C, Deighan C. Potassium disorders--clinical spectrum and emergency management. Resuscitation 2006; 70:10-25.
(34.) Satur CM, Stubington SR, Jennings A, Newton k, Martin PG, Gebitekin C et al. Magnesium flux during and after open heart operations in children. Ann Thorac Surg 1995; 59:921-927.
(35.) Mahoney BA, Smith WAD, Lo DS, Tsoi k, Tonelli M, Clase CM. Emergency interventions for hyperkalaemia. Cochrane Database Syst Rev 2005; 2:CD003235.
(36.) Rose MR, Glassman E, Spencer FC. Arrhythmias following cardiac surgery: relation to serum digoxin levels. Am Heart J 1975; 89:288-294.
(37.) Terada Y, Mitsui T, Yamaguchi I. Conduction disturbances after open heart operation in a patient receiving amiodarone. Ann Thorac Surg 1994; 58:1213-1214.
(38.) Etheridge SP, Craig JE, Compton SJ. Amiodarone is safe and highly effective therapy for supraventricular tachycardia in infants. Am Heart J 2001; 141:105-110.
(39.) Hoffman TM, Bush DM, Wernovsky G, Cohen MI, Wieand TS, Gaynor JW et al. Postoperative junctional ectopic tachycardia in children: incidence, risk factors, and treatment. Ann Thorac Surg 2002; 74:1607-1611.
(40.) Walsh EP, Saul JP, Sholler GF, Triedman Jk, Jonas RA, Mayer JE et al. Evaluation of a staged treatment protocol for rapid automatic junctional tachycardia after operation for congenital heart disease. J Am Coll Cardiol 1997; 29:1046-1053.
(41.) Smerup M, Hjertholm T, Johnsen SP, Pedersen Ak, Hansen PS, Mortensen PT et al. Pacemaker implantation after congenital heart surgery: risk and prognosis in a population-based follow-up study. Eur J Cardiothorac Surg 2005; 28:61-68.
(42.) Tucker EM, Pyles LA, Bass JL, Moller JH. Permanent pacemaker for atrioventricular conduction block after operative repair of perimembranous ventricular septal defect. J Am Coll Cardiol 2007; 50:1196-1200.
(43.) Batra AS, Wells WJ, Hinoki kW, Stanton RA, Silka MJ. Late recovery of atrioventricular conduction after pacemaker implantation for complete heart block associated with surgery for congenital heart disease. J Thorac Cardiovasc Surg 2003; 125:1291-1293.
(44.) The International Liaison Committee on Resuscitation (ILCOR) consensus on science with treatment recommendations for pediatric and neonatal patients: neonatal resuscitation.
(45.) Benson DW Jr, Sanford M, Dunnigan A, Benditt DG. Transesophageal atrial pacing threshold: role of interelectrode spacing, pulse width and catheter insertion depth. Am J Cardiol 1984; 53:63-67.
(46.) Glatter kA, Cheng J, Dorostkar P, Modin G, Talwar S, Al-Nimri M et al. Electrophysiologic effects of adenosine in patients with supraventricular tachycardia. Circulation 1999; 99:1034-1040.
(47.) Gow RM, Sanatani S, Froese N, Skippen PW. Pacemaker therapy of postoperative arrhythmias following pediatric cardiac surgery. Pediatr Crit Care Med 2009; in press.
(48.) Davignon A. ECG standards for children. Pediatric Cardiology 1980; 1:133-152.
(49.) Weindling SN, Saul JP, Gamble WJ, Mayer JE, Wessel D, Walsh EP. Duration of complete atrioventricular block after congenital heart disease surgery. Am J Cardiol 1998; 82:525527.
(50.) Krongrad E. Prognosis for patients with congenital heart disease and postoperative intraventricular conduction defects. Circulation 1978; 57:867-870.
(51.) Hokanson JS, Moller JH. Significance of early transient complete heart block as a predictor of sudden death late after operative correction of tetralogy of Fallot. Am J Cardiol 2001; 87:1271-1277.
(52.) Wang JN, Wu JM, Tsai YC, Lin CS. Ectopic atrial tachycardia in children. J Formos Med Assoc 2000; 99:766-770.
(53.) Batra AS, Chun DS, Johnson TR, Maldonado EM, Kashyap BA, Maiers J et al. A prospective analysis of the incidence and risk factors associated with junctional ectopic tachycardia following surgery for congenital heart disease. Pediatr Cardiol 2006; 27:51-55.
P. W. Skippen *, S. Sanatani ([dagger]), R. M. Gow ([double dagger]), N. Froese ([section])
Department of Critical Care, British Columbia Children's Hospital, Vancouver, British Columbia, Canada
* M.B., B.S., F.J.F.I.C.M., F.A.N.Z.C.A., F.R.C.P.C., M.H.A., Pediatric Critical Care Physician, Pediatric Intensive Care Unit.
([dagger]) M.D., F.R.C.P.C., Director, Cardiac Pacing and Electrophysiology Children's Heart Centre.
([double dagger]) M.B., B.S., F.R.A.C.P., F.C.S.A.N.Z., M.Med.Stats., Cardiologist, Division of Pediatric Cardiology, Children's Hospital of Eastern Ontario, Ontario.
([section]) M.D., F.R.C.P.C., Pediatric Cardiac Anesthetist, Pediatric Intensive Care Unit.
Address for reprints: Dr P. W. Skippen, Pediatric Intensive Care Unit, British Columbia Children's Hospital, Room 2L5, 4480 Oak Street, Vancouver, British Columbia, Canada.
Accepted for publication on March 9, 2009.
Table 1 Common postoperative arrhythmias based on mechanism and substrate Mechanism Anatomic substrate Automaticity Decreased Bidirectional Glenn, Fontan Increased All patients Increased Surgery near AVN (VSD, AVSD, ASO) Increased RAI Circuit Re-entrant Ebstein's Re-entrant HLHS Re-entrant Tetralogy of Fallot Re-entrant LTGA Re-entrant Classic Fontan Re-entrant Right atrial dilatation Re-entrant Isomerism Block LTGA, LAI Triggered Acquired QT prolongation activity Mechanism Arrhythmia Automaticity Decreased Sinus node dysfunction Increased Sinus tachycardia Increased Junctional ectopic tachycardia Increased Atrial tachycardia Circuit Re-entrant AVRT Re-entrant AVNRT Re-entrant Ventricular tachycardia Re-entrant AVRT Re-entrant IART Re-entrant Atrial flutter Re-entrant Atypical AVNRT Block Complete AV block Triggered Torsade de pointes activity Mechanism Rationale Automaticity Decreased Previous surgery in vicinity of SAN (12-14) Increased Endogenous catecholamines, metabolic state, medications all can increase sinus rate Increased AVN automaticity enhanced by trauma and endogenous catecholamines (15) Increased Accessory sinus nodes (16,17) Circuit Re-entrant Accessory pathways in 20-30% (18) Re-entrant Dual AV node physiology common in left heart obstruction (19) Re-entrant Right outflow tract conduction barriers is substrate for VT (20) Re-entrant Same as Ebstein's for systemic AV valve (21) Re-entrant Dilated atrium with scar and conduction barrier (22) Re-entrant Allows use of right atrium as macrore-- entrant pathway (23) Re-entrant Dual AVN ("Monckeborg sling") (24,25) Block Abnormal AVN or rudimentary AVN (26) Triggered Impaired repolarisation leads to after activity depolarisations (27) SAN=sinoatrial node, AVN=atrioventricular node, VSD=ventricular septal defect, AVSD=atrioventricular septal defect, ASO=atrial switch operation, RAI=right atrial isomerism, AVRT=atrioventricular re-entrant tachycardia, HLHS=hypoplastic left heart syndrome, AVNRT=atrioventricular node re-entrant tachycardia, AV=atrioventricular, LTGA=levo-transposition of the great arteries, VT=ventricular tachycardia, IART=intra-atrial re-entrant tachycardia, LAI=left atrial isomerism.
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|Author:||Skippen, P.W.; Sanatani, S.; Gow, R.M.; Froese, N.|
|Publication:||Anaesthesia and Intensive Care|
|Article Type:||Clinical report|
|Date:||Sep 1, 2009|
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