Nearly one-third of all major congenital anomalies involve cardiac defects, affecting roughly 9 per 1,000 births worldwide. 1,2 Cardiac arrhythmias are disorders of the heart's electrical system that result in abnormal heart rhythms.3 These irregularities may manifest as anomalies in heart rate, rhythm, or conduction pathways. Broadly, arrhythmias are divided into two major categories: tachyarrhythmias, which are characterized by a heart rate exceeding 100 beats per minute, and bradyarrhythmias, in which the heart rate is below 60 beats per minute. Furthermore, arrhythmias are classified according to their site of origin, with supraventricular arrhythmias arising above the ventricles and ventricular arrhythmias originating within the ventricles. Common examples include atrial fibrillation, atrial flutter, supraventricular tachycardia (SVT), ventricular tachycardia (VT), and ventricular fibrillation (VF).4,5,6,7,8,9
Postoperative arrhythmias are frequently observed in pediatric cardiac intensive care units (ICUs)10 and are associated with significant hemodynamic deterioration,11,12,13,14 which in turn increases both morbidity and mortality.14 Although these arrhythmias are generally temporary and often resolve with medical treatment, their presence in the ICU can substantially worsen a patient's condition.6,15,16,17,18
Postoperative arrhythmias in pediatric patients with congenital heart defects (CHDs) are highly diverse, presenting as either tachyarrhythmias or bradyarrhythmias. Bradyarrhythmias typically manifest as sinus bradycardia and atrioventricular blocks (AVB), whereas tachyarrhythmias encompass atrial tachycardia (including intra-atrial reentrant tachycardia and atrial flutter), junctional ectopic tachycardia (JET), and various forms of ventricular tachycardia (such as premature ventricular complexes, monomorphic VT, Torsades de Pointes, and ventricular fibrillation).8
The underlying causes of early postoperative arrhythmias include direct injury to the cardiac conduction system during surgery, as well as edema and inflammation in the myocardial tissue adjacent to the conduction pathways. In addition, factors such as ischemia–reperfusion injury associated with cardiopulmonary bypass (CPB), electrolyte imbalances, acid–base disturbances, the patient's age at the time of surgery, hemodynamic instability, pain, sedation, and the use and dosage of inotropic drugs may all contribute to both the development and frequency of early postoperative arrhythmias.11,12,13,14,15,20,21,22,23,24 In pediatric patients, these arrhythmias can be life-threatening; therefore, prompt and accurate diagnosis coupled with appropriate management is essential to prevent further complications. Although many arrhythmias resolve spontaneously or with pharmacological treatment, some cases require additional interventions, such as defibrillation or the implantation of a permanent pacemaker.5,11,12,16,17,25,26,27
Given that the reported incidence of postoperative arrhythmias varies widely, from 6.78% to 48%, obtaining a more precise estimate is crucial. Improved accuracy in incidence data could allow clinicians to better tailor monitoring and treatment strategies.6,18,19,20
Due to the lack of a clear picture of the incidence of early postoperative arrhythmias in pediatric patients with CHD, we performed a systematic review of the literature. Our aim was to assess the occurrence of dysrhythmias in the pediatric CHD population and to identify the risk factors that contribute to their development.
We searched the PubMed, Embase and Web of Science databases using the following queries: “arrythmias, pediatric, congenital heart disease, incidence”, “arrhythmias, pediatric, congenital heart disease, risk factors”, “arrhythmias, pediatric, congenital heart disease, cardiac surgery”, returning the results displayed in Figure 1. Using predefined search filters in several databases for observational studies, a number of 1,597 records were excluded, and identified references were checked for duplicates. Afterwards, titles and abstracts were screened manually for an additional removal of 324, qualifying a total of 43 articles for further evaluation. Another 27 were excluded due to missing data, absence of control group, no separate analysis of arrhythmias, or small cohorts. Finally, 16 studies were included (Table 1).
Summary of included studies
| No. | Author & year | Country | Type of study | Study period | Population size |
|---|---|---|---|---|---|
| 1 | Pfammater et al.13, 2002 | Switzerland | Prospective | July 1996 – unspecified | 172 |
| 2 | Valsangiacomo et al.7, 2002 | Switzerland | Prospective | November 1998 – January 2000 | 100 |
| 3 | Delaney et al.24, 2006 | USA | Prospective | September 2000 – May 2003 | 189 |
| 4 | Rekawek et al.12, 2007 | Poland | Prospective | January – December 2005 | 402 |
| 5 | Chaiyarak et al.22, 2008 | China | Prospective | January – December 2006 | 191 |
| 6 | Yildirim et al.19, 2008 | Turkey | Retrospective | May 2001 – December 2002 | 580 |
| 7 | Kamel et Sewielam27, 2009 | Egypt | Retrospective | September 2007 – January 2009 | 95 |
| 8 | Massin et al.26, 2010 | Belgium | Prospective | January 2007 – June 30 | 141 |
| 9 | Talwar et al.17, 2015 | India | Prospective | September 2013 – July 2014 | 200 |
| 10 | Nelson et al.25, 2018 | USA | Retrospective | January 2012 – December 2014 | 196 |
| 11 | Sahu et al.23, 2018 | India | Prospective | November 2015 – December 2016 | 369 |
| 12 | Jain et al.5, 2019 | India | Retrospective | April – July 2016 | 536 |
| 13 | Öztürk et al.11, 2021 | Turkey | Retrospective | December 2018 – November 2019 | 670 |
| 14 | Alotaibi et al.21, 2022 | Saudi Arabia | Retrospective | January 2015 – December 2020 | 821 |
| 15 | Ishaque et al.20, 2022 | Pakistan | Retrospective | January 2014 – December 2018 | 812 |
| 16 | Yasa et al.8, 2024 | Indonesia | Retrospective | January 2020 – December 202 | 92 |
Studies were included if they met the following criteria: (1) the investigation focused on the incidence of early postoperative arrhythmias; (2) it was a cross-sectional observational study; (3) the patient population consisted of individuals under 19 years of age; (4) the data pertained to patients undergoing congenital heart surgery; and (5) the study provided case numbers, means, and standard deviations, or sufficient information to calculate them.
Studies were excluded if: (1) they provided data on late postoperative arrhythmias; (2) they involved therapeutic methods other than surgical interventions; (3) the patient population consisted of individuals over 19 years of age; (4) they were determined to be of low quality; or 5) they were published before 2000.
The Newcastle–Ottawa Scale for assessing the quality of cohort studies was used to evaluate the included studies (Table 2). All studies scored a minimum of seven stars (high-quality studies).
Quality assessment using the Newcastle–Ottawa scale
| No. | Author & year | Selection | Comparability | Outcome | Total |
|---|---|---|---|---|---|
| 1 | Pfammater et al.13, 2002 | 4 | 1 | 3 | 8 |
| 2 | Valsangiacomo et al.7, 2002 | 4 | 1 | 3 | 8 |
| 3 | Delaney et al.24, 2006 | 4 | 1 | 3 | 8 |
| 4 | Rekawek et al.12, 2007 | 4 | 1 | 3 | 8 |
| 5 | Chaiyarak et al.22, 2008 | 4 | 1 | 3 | 8 |
| 6 | Yildirim et al.19, 2008 | 3 | 1 | 3 | 7 |
| 7 | Kamel et Sewielam27, 2009 | 3 | 1 | 3 | 7 |
| 8 | Massin et al.26, 2010 | 3 | 1 | 3 | 7 |
| 9 | Talwar et al.17, 2015 | 4 | 1 | 3 | 8 |
| 10 | Nelson et al.25, 2018 | 4 | 1 | 3 | 8 |
| 11 | Sahu et al.23, 2018 | 4 | 1 | 3 | 8 |
| 12 | Jain et al.5, 2019 | 4 | 2 | 3 | 9 |
| 13 | Öztürk et al.11, 2021 | 4 | 1 | 3 | 8 |
| 14 | Alotaibi et al.21, 2022 | 4 | 2 | 3 | 9 |
| 15 | Ishaque et al.20, 2022 | 4 | 1 | 3 | 8 |
| 16 | Yasa et al.8, 2024 | 4 | 2 | 3 | 9 |
All 16 articles included in the review were cross-sectional, observational studies conducted at single centers. The duration of the studies ranged from 1 to 5 years. In one study,13 initiated in 1999, no specific end date or overall time span was provided; instead, the study period was defined as the entire postoperative hospital stay for each patient, from the time of surgical intervention until discharge. Given that the length of hospital stay varied for each patient, the overall study duration would be defined as the time interval between the admission date of the first patient included in the study and the discharge date of the last patient to be discharged among all participants. Details concerning patient groups analyzed by extracted studies are presented in Table 3.
Summary of included studies
| No. | Author & year | Sample size | Arrhythmia cases (n) | Arrhythmia cases (%) | Groups | No. of patients | Age (months) | CBP time (min) | ACC time (min) |
|---|---|---|---|---|---|---|---|---|---|
| 1 | Pfammater et al.13, 2002 | 172 | 59 | 34.30% | Arrhythmia | 59 | 16.62 ± 4.79 | – | – |
| Non-arrhythmia | 113 | 33 ± 11.25 | |||||||
| 2 | Valsangiacomo et al.7, 2002 | 100 | 48 | 48.00% | Arrhythmia | 48 | 25.26 ± 53.25 | – | – |
| Non-arrhythmia | 52 | ||||||||
| 3 | Delaney et al.24, 2006 | 189 | 28 | 14.81% | Arrhythmia | 28 | 22 ± 39.7 | 189 ± 106 | 105 ± 73.6 |
| Non-arrhythmia | 161 | 109 ± 29.6 | 44 ± 22.2 | ||||||
| 4 | Rekawek et al.12, 2007 | 402 | 57 | 14.18% | Arrhythmia | 57 | 18.74 ± 39.04 | 169 ± 69.2 | 82.6 ± 37.1 |
| Non-arrhythmia | 345 | 31.23 ± 47.7 | 128.7 ± 134.9 | 53.6 ± 34.2 | |||||
| 5 | Chaiyarak et al.22, 2008 | 580 | 45 | 7.76% | Arrhythmia | 45 | 48.03 ± 45.26 | 96 (30–251) | 48 (0–147) |
| Non-arrhythmia | 146 | 38.33 ± 47.47 | 65 (20–240) | 36 (0–147) | |||||
| 6 | Yildirim et al.19, 2008 | 191 | 51 | 26.70% | Arrhythmia | 51 | 20.4 ± 27.6 | 105 .4 ± 54.1 | 56.7 ± 27.2 |
| Non-arrhythmia | 529 | – | – | – | |||||
| 7 | Kamel et Sewielam27, 2009 | 95 | 30 | 31.58% | Arrhythmia | 30 | 11 ± 2 | 105.4 ± 53.1 | 50 ± 22.5 |
| Non-arrhythmia | 65 | 16 ±3 | 80.8 ± 36.3 | 50 ± 22.5 | |||||
| 8 | Massin et al.26, 2010 | 141 | 25 | 17.73% | Arrhythmia | 25 | 2.56 ± 3.28 | 139.64 ± 51.15 | 76.20 ± 32.99 |
| Non-arrhythmia | 116 | 2.39 ± 3.40 | 113.55 ± 37.47 | 56.26 ± 24.72 | |||||
| 9 | Talwar et al.17, 2015 | 200 | 15 | 7.50% | Arrhythmia | 15 | 41.9 ± 65.4 | 108.5 ± 46.7 | 62.2 ± 21.42 |
| Non-arrhythmia | 185 | 50.7 ± 62.2 | 79.99 ± 36.5 | 50.6 ± 22.43 | |||||
| 10 | Nelson et al.25, 2018 | 196 | 18 | 9.18% | Arrhythmia | 18 | 5.9 ± 1.8 | 123 (112–187) | 74 (56–128) |
| Non-arrhythmia | 178 | 28.8 ± 24.3 | 97 (70–144) | 45 (16–80) | |||||
| 11 | Sahu et al.23, 2018 | 369 | 25 | 6.78% | Arrhythmia | 25 | 39.36 ± 42.6 | 103.6 ± 57.4 | 60.04 ± 32.8 |
| Non-arrhythmia | 344 | 37.2 ± 42 | 90.04 ± 44/7 | 55.1 ± 26.5 | |||||
| 12 | Jain et al.5, 2019 | 536 | 77 | 14.37% | Arrhythmia | 77 | 16 | – | – |
| Non-arrhythmia | 459 | ||||||||
| 13 | Öztürk et al.11, 2021 | 670 | 84 | 12.54% | Arrhythmia | 84 | 4 ± 53.99 | – | – |
| Non-arrhythmia | 586 | ||||||||
| 14 | Alotaibi et al.21, 2022 | 821 | 140 | 17.05% | Arrhythmia | 140 | – | 77 (57–99.5) | 54 (38–70) |
| Non-arrhythmia | 681 | 60 (45–81) | 45 (32–62) | ||||||
| 15 | Ishaque et al.20, 2022 | 812 | 185 | 22.78% | Arrhythmia | 185 | – | 140.4 ± 70.2 | 55.6 ± 27.4 |
| Non-arrhythmia | 627 | ||||||||
| 16 | Yasa et al.8, 2024 | 92 | 14 | 15.22% | Arrhythmia | 14 | 69.71 ± 65.71 | 171.23 ± 52.64 | 115.58 ± 34.38 |
| Non-arrhythmia | 75 | 88.78 ± 65.28 | 108.1 ± 48.44 | 73.59 ± 37.28 |
The incidence reported in the selected studies ranged from 6.78%24 to 48%7 (Table 3). Considering that the oldest studies7,13 reported the highest incidences, it can be argued that advancements in surgical techniques have contributed to the reduction in the incidence of postoperative arrhythmias, enhancing outcomes for pediatric patients undergoing heart surgery. Studies5,8,11,17,20,21,23,25 published in the last 10 years converge on reporting lower incidences between 7.50%17 and 22.78%.20 Our literature search yielded a broad spectrum of postoperative arrhythmias among patients with CHD, with considerable variability in reported incidences across studies. The most frequently reported include JET, AVB, and SVT. Additionally, junctional rhythms, VT, VF, and atrial fibrillation are also noted, though less frequently.
The spectrum of postoperative arrhythmias is notably broad, and the selected studies have reported substantial disparities in the incidence and predominance of specific arrhythmia types.
While JET and atrio-ventricular block (AVB) incidences show marked differences across studies, with the highest incidences reported by Alotaibi et al.21 and Kamel and Sewielam, 27 and the lowest by Yildirim et al.,19 the occurrence of other arrhythmias, such as junctional rhythm, VT, VF, and atrial fibrillation, is generally much lower.
Notably, the highest overall incidence of JET (25.6%) was reported by Alotaibi et al.21 and Kamel and Sewielam.27 In stark contrast, Yildirim et al.19 documented the lowest incidence at only 2.06%. Intermediate rates were observed in several other studies.5,11,13,22,24 Surgical manipulation near the crux of the heart, particularly during repairs of ventricular septal defects (VSDs), atrioventricular septal defects (AVSDs), and tetralogy of Fallot (TOF), can result in mechanical stretching, edema, or even direct injury to the atrioventricular (AV) node. This trauma may induce enhanced automaticity in the junctional tissue, leading to the high incidence of JET observed in multiple studies.21,27
Similarly, there is considerable variability among studies reporting the incidence of postoperative AVB. Alotaibi et al.21 reported the highest overall incidence at 14.6%, whereas Yildirim et al.19 found the lowest at only 1.2%; other studies5,11,13,20,27 have reported intermediate values. This variability likely reflects differences in surgical technique and the degree of exposure of the AV node during repair, as inadvertent injury to this specialized conduction tissue, especially when operating in close proximity to the AV node, substantially increases the risk for AVB.28
SVT exhibits notable variability in incidence among patients with postoperative arrhythmia. Kamel and Sewielam27 reported the highest incidence at 35.7%, whereas Alotaibi et al.21 and Valsangiacomo et al.7 observed considerably lower rates of 10% and 9%, respectively. This disparity may be partly explained by the systemic inflammatory response induced by CPB, which can lead to myocardial edema and alter the electrophysiological properties of cardiac tissue. Additionally, elevated catecholamine levels in the postoperative period further increase myocardial excitability, creating a setting in which reentrant circuits and abnormal automaticity are more easily triggered, thereby predisposing patients to SVT.28,29 Electrolyte disturbances, which are common after extensive surgery, may further modify the conduction properties of the myocardium, contributing to the genesis of JET, AVB, and SVT. Additionally, transient ischemia during surgery can alter refractoriness and conduction velocity, facilitating the development of these arrhythmias.30
By contrast, arrhythmias such as VT, VF, and atrial fibrillation typically require a more specific arrhythmogenic substrate, such as significant scarring or well-established reentrant circuits, which is less commonly created during congenital cardiac surgeries. This likely accounts for their relatively lower incidence in the postoperative period.
Despite the variability in overall incidence, most studies converge on the observation that most arrhythmias occur within the first 24 h after surgery. Alotaibi et al.21 found that 79.3% of arrhythmias manifested within the first 24 h, a finding corroborated by several other studies17,23,25,27 in which at least two-thirds of patients developed arrhythmias within this timeframe. Furthermore, Chaiyarak et al.22 provided additional detail, noting that a small subset (4.4%) of arrhythmias occurred during surgical intervention.
Nelson et al.25 added to the perspective by reporting a median arrhythmia duration of 22 h, while Jain et al.5 provided further information on early onset of dysrhythmia, noting that 92% of JET cases and most junctional escape rhythm events (84.6%) were detected within 24 h.
However, Yildirim et al.19 described arrhythmias occurring as late as 72 h post surgery, while Öztürk et al.11 noted that although most JET cases (89.5%) were identified within 24 h, a few were detected 72 h postoperatively. Kamel and Sewielam27 documented a case that manifested beyond 48 h after surgery. The delayed onset of arrhythmias during the early postoperative period can be attributed to several factors, including the body's inflammatory response, hemodynamic changes, electrolyte imbalances, pain and stress, and the effects of medications administered during and after surgery.30,31
The variability in conduction system anatomy across different CHDs can be an easily overlooked factor in the development of postoperative arrhythmias. In VSDs, for instance, Milo et al.32 established marked differences in conduction pathways among VSD subtypes. In perimembranous VSDs, conduction tissue typically runs inferior to the defect, but its distance from the VSD crest can vary from as little as 2 mm to over 5 mm, depending on the defect's extension. In contrast, muscular inlet VSDs—with an intact membranous septum—consistently exhibit conduction running superiorly and more than 5 mm away.32,33 Furthermore, anatomical variations, such as a straddling tricuspid valve, may displace the AV node inferiorly.34 These differences heighten the risk of unintentional injury during surgical repair. Notably, our review suggests that VSD repairs are associated with a relatively lower incidence of postoperative arrhythmias; however, several selected studies reported a relatively low incidence of postoperative arrhythmias associated with VSD repairs: Alotaibi et al.21 reported that 18.6% of arrhythmia cases occurred after VSD repair, while Chaiyarak et al.22 observed only a 6.5% incidence of AVB; these findings were supported by others as well.5,17
In TOF, Dickinson et al.35 reported significant variability in conduction anatomy. Although most TOF specimens display an AV bundle running posteriorly or inferiorly, sufficiently distant from the VSD to minimize risk, approximately 30% of cases with perimembranous extension exhibit conduction tissue positioned on or near the posterior or inferior VSD crest, which increases its susceptibility to surgical trauma.35 This observation was supported by Nelson et al.,25 who reported a 33% incidence of arrhythmias in TOF, and Kamel and Sewielam,27 who found 39.2% of arrhythmia cases were associated with TOF.
AVSDs further complicate surgical management. Lev36 described that in AVSDs the atrioventricular node and bundles are displaced posteroinferiorly, originating near the coronary sinus and coursing along the left aspect of the inferior VSD crest, which requires meticulous suture placement to avoid this particular region. Variations in the location of the His bundle have also been reported.8 Supporting these findings, Ishaque et al.20 documented a striking 64.3% incidence of arrhythmias (predominantly JET) following AVSD repair, whereas Kamel and Sewielam27 noted that AVSD repairs in cyanotic patients accounted for 21.4% of arrhythmia cases.
In congenitally corrected transposition of the great arteries (ccTGA), bulboventricular looping significantly influences conduction system orientation. Anderson et al.37,38,39 found that in L-looped ventricles, conduction typically runs anterosuperiorly relative to the VSD, whereas in D-looped ventricles it is positioned posteroinferiorly. Additional factors, such as septal alignment and the presence of a Monckeberg sling, further modulate the conduction location.37,38,39,40
In summary, the heterogeneous anatomy of the conduction system in CHDs—particularly in VSDs, TOF, AVCDs, and ccTGA—creates substantial challenges during surgical repair. Although there is some conflicting evidence regarding the risk associated with VSD repairs, our findings align with the literature32,33,34,35,36,37,38,39,40,41 in establishing an obvious association between surgical manipulation near critical conduction tissue and the development of early postoperative arrhythmias, especially in TOF, AVSDs, and ccTGA.
Younger age and lower body weight have been repeatedly linked to postoperative arrhythmias, likely due to a more vulnerable myocardium. Several studies25,26,27 identified age as a risk factor; both Öztürk et al.11 and Jain et al.5 noted age <1 year as an independent risk factor (OR = 1.96; 95% CI 1.18–3.24; p = 0.009), most likely due to an immature cardiac conduction system, whose ion channel expression and autonomic regulation render the heart more susceptible to electrical instability, particularly when exposed to surgical manipulation. By contrast, Yildirim et al.19 observed a nonsignificant trend in the 0–6-month group (p = 0.351), while Yasa et al.8 (MW = 0.794; p = 0.427) reported no significant impact of age.
A retrospective Egyptian study from 200827 found that patients with arrhythmias were both younger (11 ± 2 months vs. 16 ± 3 months, p < 0.05) and lighter (8 ± 1.5 kg vs. 11.5 ± 1 kg, p < 0.05), a finding supported a decade later by Nelson et al.,25 while Valsangiacomo et al.7 identified only lower weight as independently significant (p < 0.05), supporting the hypothesis that lower weight, indicative of reduced myocardial mass, compromises the heart's ability to withstand the hemodynamic fluctuations and inflammatory responses induced by surgery, thereby increasing the risk of arrhythmias. Other studies17,20,21,22,23 found no significant associations between arrhythmias, younger age, and lower weight.
Arrhythmias following congenital heart surgery show distinct associations with specific repair types. The highest incidence is observed in complex procedures, particularly AVSD and TOF repairs, which inherently involve greater manipulation near the AV node. For example, Ishaque et al.20 reported a 64.3% incidence of arrhythmias (primarily JET) after AVSD repair, while Nelson et al.25 documented rates of 33% in TOF and 28% in AVSD repairs. Kamel and Sewielam27 further emphasized that in cyanotic patients, TOF and AVSD repairs accounted for 39.2% and 21.4% of arrhythmia cases, respectively.
By contrast, VSD repairs tend to have a lower association with arrhythmias. Alotaibi et al.21 reported that 18.6% of arrhythmia cases occurred after VSD repair, and Chaiyarak et al.22 observed only 6.5% AVB in septal defect repairs. Other studies5,17 support these findings, linking VSD repair and intraventricular tunnel procedures with a relatively lower, albeit still significant, risk of arrhythmias.
Additional studies8,11,12,17 further substantiate these trends, highlighting that factors such as longer extracorporeal circulation times and the extent of surgical manipulation contribute to the observed variability. Thus, while AVSD and TOF repairs are most frequently associated with high arrhythmia rates, VSD repairs typically exhibit lower incidences, with intermediate values reported across various studies.
Complex procedures typically require extensive myocardial manipulation and are associated with prolonged CPB and aortic cross-clamp (ACC) times. These factors predispose the myocardium to ischemia, an exaggerated inflammatory response, and electrolyte imbalances, all of which destabilize cardiac electrophysiology. This concept is supported by studies5,11,20 demonstrating that higher RACHS scores (≥3 or ≥4) and Aristotle levels (≥3) are independent predictors of postoperative arrhythmias. Furthermore, Kamel and Sewielam27 observed that complex corrective surgeries, such as TOF and AVSD repairs, have a higher incidence of arrhythmias compared to palliative procedures, while Rekawek et al.,12 Sahu et al.,23 and Nelson et al.25 confirmed that increased case complexity, as measured by the Aristotle score, is strongly associated with postoperative arrhythmias. Additionally, redo operations significantly elevate the risk of arrhythmias, as found by a retrospective study27 in which 14.2% of patients in the arrhythmic group had undergone redo procedures, compared to only 1.7% in the nonarrhythmic group. This disparity is likely attributable to the scar tissue and fibrosis from previous interventions, which predispose the myocardium to conduction abnormalities.
The immaturity of the autonomic nervous system in younger patients can result in an exaggerated catecholamine surge during surgical stress. This heightened sympathetic activation further destabilizes the myocardium, increasing its susceptibility to arrhythmias, an effect further amplified by the additional stress of CPB.28 Consequently, prolonged CPB and ACC times are consistently linked to early postoperative arrhythmias. For example, Alotaibi et al.21 found each extra minute of CPB raised the odds of arrhythmia (OR = 1.014; 95% CI 1.008–1.019; p = 0.0001) and a longer ACC time also increased the risk (OR = 1.011; 95% CI 1.003–1.019; p = 0.009). Similarly, Kamel and Sewielam27 noted that patients with arrhythmia had longer CPB times (105.4 ± 53.1 min vs. 80.8 ± 36.3 min, p < 0.05), a finding supported by Valsangiacomo et al.7 (p < 0.05). Chaiyarak et al.22 demonstrated that CPB times >85 min increased the odds of arrhythmias (OR = 4.87; 95% CI 2.34–10.12; p < 0.001; sensitivity 70.2%; specificity 67.4%) and JET (OR = 6.79; 95% CI 2.03–22.68; p = 0.001; sensitivity 83.3%; specificity 62.4%). Other studies also reported longer CPB times in the arrhythmia groups. For instance, Delaney et al.24 observed 189 min vs. 109 min (p < 0.05), Nelson et al.25 124 min vs. 97 min (p < 0.05), and Pfammater et al.13 found that the incidence of arrhythmia in VSD repairs rose from 7% (<50 min extracorporeal circulation (ECC)) to 39% (>50 min ECC). Ishaque et al.20 and Öztürk et al.11 identified CPB cutoffs at >120 min and 140 min, respectively, while Yasa et al.8 reported longer CPB times as significant (p = 0.034). By contrast, Jain et al.5 and Rekawek et al.12 did not find CPB time to be an independent factor in multivariate analysis (p = 0.056 and p = 0.9, respectively), and Sahu et al.23 noted no significant difference (p < 0.16).
Regarding ACC time, Pfammater et al.13 reported that in VSD repairs, the incidence of arrhythmia increased from 5% (<30 min) to 47% (30–60 min, p < 0.01). Children with arrhythmias had longer ECC (68 ± 17 min vs. 53 ± 14 min; p < 0.01) and ACC times (42 ± 15 min vs. 31 ± 9 min; p < 0.01). Similar trends were seen in TOF and CAVC repairs. Delaney et al.24 noted ACC times of 105 ± 73.6 min in patients with arrhythmia vs. 44 ± 22.2 min in patients without arrhythmia (p < 0.05); these findings are in agreement with those of Massin et al.26 (p < 0.001) and Jain et al.5 (ACC >67 min, p = 0.024). However, Ishaque et al.20 found that an ACC of >60 min was not significant (OR = 1.97; 95% CI 0.68–2.66; p = 0.234). Valsangiacomo et al.,7 Öztürk et al.,11 and Kamel and Sewielam27 did not evaluate ACC time.
Hemodynamic instability is a critical risk factor for early postoperative arrhythmias. The stress from hemodynamic compromise triggers an exaggerated sympathetic response and increased catecholamine release, which enhances myocardial automaticity and irritability.42 Alotaibi et al.21 demonstrated this association with an OR of 2.467 in univariate analysis and a persistent significant relationship in multivariate analysis (OR = 1.722; 95% CI 1.104–2.884; p = 0.018). Additionally, Kamel and Sewielam27 observed that patients who require high inotropic support, have hypotension in the ICU, and need prolonged ventilation are more susceptible to arrhythmias. Sahu et al.24 further reported significant links with hypotension and tachycardia, likely because systemic hypoperfusion leads to metabolic acidosis and electrolyte imbalances (particularly of potassium and calcium) that destabilize cardiac electrophysiology. 43 Nelson et al.25 noted that arrhythmic patients had lower early extubation and higher reintubation rates compared to nonarrhythmic patients. Moreover, Yildirim et al.19 documented a high incidence of hemodynamic instability (73.2%) and a 29.4% mortality rate among these patients, although targeted therapy can mitigate these adverse effects, as shown by Valsangiacomo et al.7
Electrolyte imbalances are known to predispose the myocardium to arrhythmias by disturbing normal electrophysiological processes. In the postoperative setting, children with congenital heart disease are especially vulnerable to these disturbances due to factors such as hemodilution during CPB, renal function alterations, and the systemic inflammatory response induced by surgery.29,30,43 These factors can lead to significant electrolyte shifts, exacerbating myocardial instability and increasing the propensity for arrhythmias, as reported by Alotaibi et al.21 and Yasa et al.8 Although some studies17,19,23,25,27 have reported conflicting results regarding the impact of specific electrolyte levels, there is evidence that supports the notion that disturbances in electrolyte homeostasis remain a risk factor for postoperative arrhythmias in this high-risk pediatric population.
High inotropic support, as reflected by increased vasoactive inotropic scores (VIS), was another incriminated risk factor for arrhythmias. Kamel and Sewielam27 reported that 32.1% of arrhythmic cases required high inotropic support on leaving the operating room compared to only 5.2% in the nonarrhythmic group (p < 0.01). This finding is further supported by Sahu et al.,23 who demonstrated that a higher Werknovsky inotropic score is significantly associated with the occurrence of arrhythmia (arrhythmia group: OR = 20; 95% CI 5–52 vs. non-arrhythmia group: OR = 15; 95% CI 0–59; p = 0.02). Additional studies11,20 identified VIS as a strong independent risk factor, likely due inotropic agents increasing myocardial irritability and automaticity by affecting cardiomyocyte membranes. By contrast, Nelson et al.25 did not find a significant difference in VIS between arrhythmic and nonarrhythmic groups (p = 0.787).
From a geographical perspective, a higher incidence of postoperative arrhythmias was predominantly reported in developed countries during the early 2000s,7,13 with a downward trend observed in subsequent years.25,26 Given that older studies reported the highest incidences, it can be argued that technological progress and the refinement of surgical techniques have contributed to the reduction of the incidence of postoperative arrhythmias, thereby improving outcomes for pediatric patients undergoing cardiac surgery.
On the other hand, while in the first decade of the 21st century studies on the incidence of postoperative arrhythmias are largely absent in certain Asian and African countries, likely due to limited access to advanced cardiac surgical interventions, recent years have seen a notable shift. The economic development of these regions has contributed to significant improvements in medical infrastructure and the capacity to perform complex surgeries for CHD. Consequently, this progress has led not only to an increase in the number of published studies originating from these countries but also to the reporting of relatively high incidences8,20,21 of postoperative arrhythmias.
However, the discrepancies in reported postoperative arrhythmia incidence mostly stem from variations in definitions, monitoring methods, and patient selection. For instance, while some studies19,23 define arrhythmias as any non-sinus rhythm lasting over 30 s or requiring intervention, others, such as Delaney et al.,24 include only events that require active treatment. Similarly, inconsistency exists in classifying SVT: some investigators17,25 group all SVT subtypes under atrial tachycardia; others, such as Pfammater et al.,13 distinguish between atrioventricular reentrant tachycardia and atrial flutter, while others23,27 define SVT as a narrow complex tachycardia with one-to-one AV conduction. Likewise, criteria for AVB vary, with some studies7,11,21 differentiating between second- and third-degree AVB and others22,23 focusing solely on complete AVB.
Incidence differences also arise from arrhythmia selection criteria, duration of monitoring, and the patient case mix. For example, Rekawek et al.12 and Delaney et al.24 reported intervention-requiring arrhythmias in 14–15% of patients, whereas Alp et al.44 and Grosse-Wortmann et al.45 documented higher incidences when minor rhythm abnormalities were included, although these rates declined significantly when benign changes were excluded.
Surgical factors further contribute to these disparities. Intraoperative hemodynamic instability, along with prolonged CPB and ACC times, predisposes the myocardium to ischemia, reperfusion injury, and electrolyte shifts, all of which destabilize cardiac electrophysiology.19,21,24,36 These effects are compounded by an exaggerated catecholamine surge in response to stress47 and by direct surgical trauma from cannulation, suturing near the conduction system, and rapid intracardiac pressure changes.7 Moreover, corrective and redo surgeries elevate arrhythmia risk due to additional tissue trauma and inflammatory responses.27,47
Specific mechanisms also vary by procedure, according to the literature. For instance, in TOF repairs, high rates of JET and SVT have been attributed to His bundle trauma from right atrial traction.48 In patients with single ventricle physiology, inherent conduction abnormalities, prolonged CPB, and redo operations further increase the risk of JET. Jacobs et al.49 observed that early arrhythmias were associated with myocardial swelling, unstable hemodynamics, high inotrope doses, and metabolic disturbances, while Nelson et al.25 suggested that para-Hisian injury leading to abnormal automaticity may precipitate JET and subsequent complete heart block. Additionally, Sahu et al.24 linked longer surgical duration, elevated serum lactate, hypotension, and tachycardia to myocardial insults, and other studies50,51,52,53 have associated hypomagnesemia with JET.
Collectively, these findings highlight the complex interplay between methodological differences and pathophysiological factors in determining the incidence of postoperative arrhythmias in children with CHD.
With a few exceptions that had a medium size cohort, most of the studies had relatively small sample sizes, which may have constrained the statistical power to detect less frequent arrhythmic events and limited the ability to conduct comprehensive subgroup analyses. Furthermore, the study populations were often clinically diverse, including a wide range of CHDs varying in anatomical complexity, surgical approaches, and postoperative management strategies. This clinical diversity may have introduced important confounding factors, including inconsistencies in inclusion criteria, such as differences in age at the time of surgery, type of surgical intervention, use of cardiopulmonary bypass, preoperative clinical status, and postoperative care protocols. This diversity, while representative of real-world pediatric cardiology practice, complicates the identification of specific risk factors for postoperative arrhythmias and makes it more difficult to isolate specific associations. Larger-scale studies with more homogenous subgroups are needed to confirm these findings and better define risk factors for postoperative arrhythmias.
The identification of incidence patterns, risk factors, and vulnerable subgroups in children with CHD has important implications for clinical practice, particularly in the prevention and management of postoperative arrhythmias. These insights may support more refined perioperative risk stratification, allowing surgical teams to adapt intraoperative techniques accordingly and enabling clinicians to consider early correction of electrolyte disturbances or the use of prophylactic antiarrhythmic agents in selected cases.
Nevertheless, several important questions remain unanswered. Reported incidence rates vary widely, and the true incidence of specific postoperative arrhythmias within individual CHD subtypes is still difficult to determine, in part due to variations in study design. Additionally, the role of intraoperative factors and preexisting conditions, such as genetic syndromes, requires further research. Addressing these gaps might require further studies based on large, multicenter cohorts that examine individual arrhythmia types rather than combining diverse outcomes. Future research should also explore the utility of intraoperative conduction mapping and its role in minimizing conduction system injury. Combined with genetic and clinical profiling, it could provide valuable insights into arrhythmia mechanisms. Integrating these variables into a comprehensive risk stratification score may facilitate early identification of high-risk patients, improving outcomes in this vulnerable population.