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Bradycardia in children

Bradycardia in children
Literature review current through: Jan 2024.
This topic last updated: Mar 20, 2023.

INTRODUCTION — Bradycardia is defined as a heart rate below the normal range for age (table 1). Bradycardia is caused by intrinsic dysfunction or injury to the heart's conduction system or by extrinsic factors acting on a normal heart and its conduction system. Children who have bradycardia with poor perfusion or shock need immediate medical attention (algorithm 1). In patients with non-life-threatening symptoms, the management is dependent upon the severity of symptoms, specific conduction defect, and whether there is underlying congenital heart disease.

The causes, evaluation, diagnosis, management, and outcome of bradycardia in children will be discussed here. Other forms of irregular heart rate in children and principles of pediatric advanced life support are discussed separately. (See "Irregular heart rhythm (arrhythmias) in children" and "Pediatric advanced life support (PALS)".)

DEFINITION — The normal range for heart rate varies with age (table 1) [1]. Younger patients have higher heart rates that decrease to adult values by the late teenage years.

Various thresholds are used to define bradycardia in children. For the purpose of this topic review, we define bradycardia as a heart rate measured in the awake state that is below the normal range for age (ie, <100 beats per minute [bpm] for infants, <80 bpm for toddlers and young children, <70 for school age children, and <60 for adolescents).

Alternate definitions are as follows:

Criteria used in automated interpretation of pediatric 12-lead electrocardiograms are generally based on the lower limit of normal (2nd percentile) for age [2-4]:

0 to 3 months – <126 bpm

3 to 6 months – <116 bpm

6 to 12 months – <106 bpm

1 to 3 years – <97 bpm

3 to 5 years – <77 bpm

5 to 8 years – <64 bpm

8 to 12 years – <59 bpm

12 to 16 years – <53 bpm

Criteria used in 24-hour ambulatory monitoring include slower heart rates that occur normally during sleep [5-8]:

Newborns to 2 years – <60 bpm while asleep and <80 bpm while awake

2 to 6 years – <60 bpm

6 to 11 years – <45 bpm

Adolescents >11 years – <40 bpm

Adolescents >11 years who are well-trained athletes – <30 bpm

PHYSIOLOGY — Heart rate is controlled by both the cardiac conduction system and the nervous system:

Conduction system – The role of the cardiac conduction system is to initiate and conduct the electrical signal that controls and coordinates atrial and ventricular contraction, as reflected in the electrocardiogram (ECG) (figure 1) [9]. The components of the conduction system include the sinus node, atrioventricular (AV) node, and His-Purkinje system (His bundle) (figure 2).

The sinus node is the pacemaker of the heart and is located in the sulcus terminalis at the junction of the superior vena cava and the right atrium. Specialized cells (nodal or dominant cells) within the sinus node depolarize spontaneously, which initiates an electrical impulse that spreads to the AV node and through the atria, resulting in bilateral atrial contraction [5]. At the AV node, the impulse is conducted through to the bundle of His. The His bundle courses through the region of the membranous septum and divides thereafter into the right and left bundle branches. Electrical activation through an intact His bundle and bundle branches results in nearly simultaneous contraction of the right and left ventricles. (See "Normal sinus rhythm and sinus arrhythmia", section on 'Anatomy'.)

Nervous system – Both the parasympathetic and sympathetic nervous system innervate the cardiac conduction system:

Increased parasympathetic tone via the vagus nerve both decreases sinus node pacing rate and slows the AV node conduction leading to a decrease in heart rate. A very strong vagal response can transiently depress sinus node depolarization (sinus pause) or block transmission through the AV node (complete AV block). (See 'Hypervagotonia' below.)

Increased sympathetic tone increases sinus node pacing leading to an increase in heart rate.

CAUSES OF BRADYCARDIA — Bradycardia may be caused by intrinsic dysfunction or injury to the heart's conduction system or by extrinsic factors acting on a normal heart and its conduction system (table 2).

The most common causes of bradycardia in children are [5]:

Increased vagal tone – Hypervagotonia (exaggerated vagal activity) slows the pacing rate of the sinus node and slows the conduction time through the atrioventricular (AV) node. (See 'Hypervagotonia' below.)

Medications – Many medications can cause bradycardia (table 3) by direct effects on the sinus or AV node (eg, beta-adrenergic blockers, calcium channel blockers), indirect effects through the nervous system (eg, opioids), or both direct and indirect effects (eg, clonidine).

Corrective surgery of congenital heart disease – Injury from surgery or catheterization is the most common cause of intrinsic damage to the conduction system in children. Bradycardia is also seen in some patients with underlying congenital defects prior to surgery. (See "Atrial arrhythmias (including AV block) in congenital heart disease".)

There are two main mechanisms and sites for the development of bradycardia:

Sinus bradycardia – At the sinus node, the depolarization rate is decreased below the lowest normal heart rate values set for age (see 'Sinus bradycardia' below)

AV node block – Conduction of the electrical impulse is either delayed or blocked at the AV node or the bundle of His (see 'Atrioventricular heart block' below)

CLINICAL PRESENTATION

Unstable patients — In patients with severe bradycardia, cardiac output may be insufficient, leading to poor systemic perfusion, shock, and, ultimately, cardiorespiratory arrest. Children who have bradycardia with poor perfusion or hypotension require immediate cardiopulmonary resuscitation. (See 'Acute management of patients with poor perfusion' below.)

Severe bradycardia can be due to both sinus and atrioventricular (AV) node dysfunction. This most commonly results from hypoxemia, hypotension, and metabolic acidosis; however, intrinsic conduction abnormalities (eg, complete heart block) can also cause severe bradycardia [10]. (See 'Causes of bradycardia' above.)

Stable patients — Patients with milder degrees of bradycardia most commonly are asymptomatic [5,11]. Symptoms, when present, differ based upon age of the patient and whether there is underlying cardiac disease:

Infants and young children – Dizziness and syncope are difficult to ascertain in infants and preverbal young children. Thus, symptomatic patients at this age often present with nonspecific symptoms of poor feeding and lethargy. Syncope and seizure-like episodes may occur if cerebral perfusion is abruptly decreased due to a slow heart rate [12,13].

Children and adolescents – Among children and adolescents, bradycardia can present with fatigue, exercise intolerance, dizziness, and/or syncope [11,14].

Underlying congenital heart disease – In children with underlying congenital cardiac disease, bradycardia most commonly does not produce any symptoms [5,11]. However, this group is more susceptible to having symptomatic bradycardia as they may be less able to tolerate a low heart rate due to underlying compromised cardiac function.

EVALUATION — The evaluation begins with a rapid assessment to identify signs of respiratory or circulatory compromise. Children with signs of poor perfusion require immediate medical management, which precedes additional evaluation and testing. (See "Initial assessment and stabilization of children with respiratory or circulatory compromise".)

In children with bradycardia not associated with signs of hemodynamic compromise, a comprehensive history and physical examination should be performed. In addition, an electrocardiogram (ECG) is performed to identify the type of conduction abnormality.

History — The history should include the following elements, which are aimed at identifying possible causes of bradycardia (table 2):

History of exposure to medications that cause bradycardia (table 3), including prescribed medications as well as possible accidental ingestions

Family history of syncope or sudden cardiac death

History of cardiac disease

Past episodes of syncope, dizziness, and/or unexplained seizures

Physical examination — Important elements of the physical examination include:

Heart rhythm – An irregular heartbeat that arises from a pause in an otherwise regular rhythm suggests the possibility of sinus node dysfunction or second-degree atrioventricular (AV) block

Abnormal heart sounds – The presence of a heart murmur or gallop may suggest underlying congenital heart disease or other cardiac pathology

Cardiac tests — The following tests are useful in the evaluation of patients with bradycardia:

ECG – A 12-lead ECG should be obtained in children found to have bradycardia on physical examination and in those with concerning symptoms (ie, syncope, dizziness, and/or unexplained seizures). The 12-lead ECG will often help determine the type of rhythm abnormality, although its use may be limited by the occurrence of bradycardia as a transient event. (See 'Identifying the type of rhythm abnormality' below.)

Ambulatory ECG monitoring – Ambulatory monitoring for children with bradycardia may be performed for any of the following reasons:

Evaluation of second- or third-degree AV block detected by 12-lead ECG

Evaluation of physiologic heart rate response in patients with syncope/near-syncope or other concerning symptoms, in cases where bradycardia, sinus node dysfunction, or heart block is suspected as the etiology

Evaluation of genetic or metabolic conditions predisposing to bradycardia (eg, long QT syndrome) (see "Congenital long QT syndrome: Diagnosis")

Evaluation of congenital heart lesions and/or postoperative conditions predisposing to bradycardia (eg, Fontan procedure) (see "Atrial arrhythmias (including AV block) in congenital heart disease", section on 'Bradycardias')

Monitoring after initiation of heart rate slowing medication

The Holter monitor is a commonly used device for ambulatory ECG monitoring in children. It provides a continuous rhythm recording from adhesive electrodes for a minimum of 24 or 48 hours. It uses a small, lightweight, battery-operated electromagnetic tape recorder or digital recorder that records two or three channels of ECG data, including minimum, average, and maximum heart rate and longest pause in heart rate.

Other ambulatory ECG monitors are available and may be useful for patients with paroxysmal symptoms. These monitors include cardiac event recorders, which can be either looping (historical ECG data) or nonlooping.

For longer-term monitoring, there are wearable patches that can provide data for up to 14 days [15]. Insertable cardiac monitors may also be used for long-term monitoring in select patients [16].

Technologic advancements have expanded the types of wearable monitors on the market and include devices such as smartphone wireless ECG monitors and true wearables, such as the Apple Watch [17,18].

Additional details regarding ambulatory ECG monitoring are provided separately. (See "Ambulatory ECG monitoring".)

Echocardiogram – Although rarely required in the evaluation of children with asymptomatic sinus bradycardia, transthoracic echocardiography may be useful in certain patients in order to identify structural abnormalities and to assess function.

Indications for echocardiography in children with bradycardia may include [19]:

Syncope with abnormal ECG findings

Syncope in a patient with family history of sudden cardiac death or cardiomyopathy

Exertional syncope

Follow-up evaluation of children with chronic bradycardia to assess for progressive ventricular enlargement

Exercise stress testing – Exercise stress testing is not needed in making the diagnosis of bradycardia. However, it is commonly used to determine heart rate response with activity (chronotropic competence). It is helpful in differentiating abnormal cardiac conduction from hypervagotonia, as the former fails to respond to exercise, while the latter is able to achieve normal peak heart rates. Chronotropic incompetence (the inability to appropriately respond to stress) may be an indication for permanent pacemaker therapy. (See "Exercise ECG testing: Performing the test and interpreting the ECG results".)

Invasive electrophysiology testing – Invasive electrophysiology testing is rarely required to make the diagnosis. It may be helpful if the mechanism for the arrhythmia remains unclear or if symptoms suggest the presence of a potentially life-threatening arrhythmia [20]. (See "Invasive diagnostic cardiac electrophysiology studies".)

IDENTIFYING THE TYPE OF RHYTHM ABNORMALITY — Based upon the electrocardiogram (ECG) findings, the type of rhythm abnormality can be determined. This allows for more focused evaluation and treatment.

Sinus bradycardia — Sinus bradycardia is present when there is a normal sinus-appearing P wave (waveform 1) but the rate is below the normal range for age (table 1).

Sinus bradycardia may be accompanied by sinus pause or arrest, documented by the sudden absence of an expected sinus P wave. Sinus pause or absence is due either to failure to generate a sinus node depolarization or failure of a generated sinus node depolarization to exit the sinus node and enter the atria.

Sinus bradycardia can commonly be seen in normal asymptomatic children with a benign course and without any apparent underlying pathology. (See 'Asymptomatic bradycardia in healthy children' below.)

Physiologic disturbances such as severe hypoxemia, hypotension, and/or metabolic acidosis can cause sinus bradycardia.

Sinus bradycardia may also be due to an abnormality, impairment, or injury of the sinus node. This is referred to as sinus node dysfunction and is most often seen in postoperative patients with congenital heart disease (CHD). (See 'Sinus node dysfunction' below.)

Hypervagotonia — Bradycardia induced by exaggerated vagal activity is usually transient and triggered by a precipitating event. Examples of common triggers include:

Nasopharyngeal or esophageal stimulation (eg, placement of nasogastric or endotracheal tubes).

Breath-holding spells [21,22] – In an older study of 58 children with pallid breath-holding spells, ocular compression triggered sinus pause of greater than two seconds in almost 80 percent of patients and greater than four seconds in 55 percent of patients. However, applying ocular pressure as a diagnostic test is no longer recommended, due to the risk of injury to the eye [22]. (See "Nonepileptic paroxysmal disorders in infancy", section on 'Breath-holding spells'.)

Gastroesophageal reflux (GER) and vomiting – GER is commonly cited as an etiology for bradycardia in premature neonates. However, a study in preterm infants (average gestational age 29.4 weeks) showed that bradycardia events were preceded by GER in only 2.9 percent of cases [23]. (See "Gastroesophageal reflux in premature infants" and "Gastroesophageal reflux in infants".)

Coughing.

Obstructive sleep apnea – Studies of young adults with obstructive sleep apnea have demonstrated severe bradycardia (heart rates below 30 beats per minute [bpm]) and asystole of 10 seconds due to enhanced vagal tone. (See "Obstructive sleep apnea and cardiovascular disease in adults".)

In addition, vagally mediated bradycardia may occur due to:

Parasympatheticomimetic drugs and toxins (table 3) [5] – In neonates, bradycardia can occur due to maternal exposure to medications (eg, beta blockers) in late pregnancy [24]

Increased intracranial pressure [25] (see "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis")

In hypervagotonia-induced bradycardia, simultaneous atrioventricular (AV) nodal dysfunction may also occur and contribute to symptoms. The combination of the slow heart rate and an associated decline in peripheral vascular resistance are often sufficient to produce presyncope or syncope. The evaluation and management of individuals with neurally mediated (reflex) syncope is discussed separately. (See "Reflex syncope in adults and adolescents: Clinical presentation and diagnostic evaluation".)

Athletes — Most well-trained endurance athletes have resting sinus bradycardia that has traditionally been attributed to increased vagal tone. However, in clinical studies in endurance athletes, atropine and propranolol failed to alter heart rate. This suggests that in these patients the intrinsic physiology of the sinoatrial node may be altered rather than be attributable to changes in vagal tone. (See "Athletes with arrhythmias: Electrocardiographic abnormalities and conduction disturbances".)

Sinus node dysfunction — In sinus node dysfunction (waveform 2), there is inappropriate sinus bradycardia or chronotropic incompetence (failure to appropriately elevate the heart rate in response to physiologic stress). In addition to sinus bradycardia, other findings associated with nodal dysfunction include severe sinus pauses, tachycardia/bradycardia syndrome, sinus node reentry tachycardia, and sinoatrial exit block. (See "Sinus node dysfunction: Epidemiology, etiology, and natural history".)

Causes are most commonly related to CHD or acquired heart disease, though a number of other associations have been reported. These include the following:

Congenital heart disease – Sinus node dysfunction has been seen in a variety of CHD lesions, most commonly atrial septal defects. Concomitant AV nodal dysfunction is also observed in patients with atrial septal defects [11,26,27]. (See "Atrial arrhythmias (including AV block) in congenital heart disease" and "Isolated atrial septal defects (ASDs) in children: Classification, clinical features, and diagnosis".)

Other CHDs associated with sinus node dysfunction include AV canal defect, pulmonary stenosis, ventricular septal defect, single ventricle with heterotaxy (particularly the "polysplenia" type), and transposition of the great arteries [11,28].

Sinus node dysfunction and associated atrial arrhythmias occur after surgical repair of congenital lesions. This is found most commonly in repairs to the atrial wall that injure the sinus node, sinus node artery, or innervation of the sinus node [11,27,29-31]. The incidence is highest in patients with transposition of the great arteries with Mustard or Senning procedures [29,30].

Myocardial disease – Much less commonly, acquired or familial myocardial diseases such as cardiomyopathy, inflammatory diseases (myocarditis and pericarditis), or ischemic diseases can cause sinus node dysfunction. Though ischemic disease is uncommon in children, cardiac conduction abnormalities have been found in patients with Kawasaki disease [30]. (See "Familial dilated cardiomyopathy: Prevalence, diagnosis and treatment" and "Clinical manifestations and diagnosis of myocarditis in children" and "Cardiovascular sequelae of Kawasaki disease: Clinical features and evaluation".)

Myocardial ischemia due to hypoxemia or hypotension is a cause of sinus nodal dysfunction that requires immediate attention. (See 'Acute management of patients with poor perfusion' below.)

Hypothermia. (See "Hypothermia in children: Clinical manifestations and diagnosis", section on 'Pathophysiology'.)

Medications – Medications that may cause sinus node dysfunction include:

Digitalis

Beta blockers (eg, propranolol)

Calcium channel blockers (eg, verapamil)

Amiodarone

Lithium

Clonidine

These drugs should be used with caution in pediatric patients with careful monitoring. Children who have had corrective cardiac surgery are at even greater risk for sinus node dysfunction when these medications are used.

Familial – Familial bradycardia is a rare disorder. There are multiple case reports describing families with an autosomal dominant pattern of inheritance [32-34]. In these reports, syncope has been associated with the bradycardia. A severe form of bradycardia called atrial standstill, in which there is absence of atrial activity, has been reported to have a familial pattern of inheritance [35]. Mutations in the cardiac sodium channel gene SCN5A may be responsible for at least some familial cases [36].

Long QT syndrome – The sinus node dysfunction may be due to the cardiac sodium channel gene defect, which underlies some forms of the long QT syndrome. (See "Congenital long QT syndrome: Epidemiology and clinical manifestations", section on 'Bradycardia'.)

Right atrial tumors [37].

Anorexia [38]. (See "Eating disorders: Overview of epidemiology, clinical features, and diagnosis".)

Neonatal lupus [39]. (See "Neonatal lupus: Epidemiology, pathogenesis, clinical manifestations, and diagnosis".)

Apnea and bradycardia of prematurity [40]. (See "Pathogenesis, clinical manifestations, and diagnosis of apnea of prematurity".)

Atrioventricular heart block — AV block is defined as a delay or interruption in the transmission of an atrial impulse to the ventricles due to an anatomical or functional impairment in the conduction system. The conduction can be delayed, intermittent, or absent. Heart block is categorized into first-degree (slowed conduction without missed beats), second-degree (intermittent conduction with missed beats), and third-degree or complete AV block (absent conduction).

First-degree atrioventricular block — In first-degree AV block, the PR interval is greater than the upper limits of normal for age (waveform 3). The PR interval is both age and rate dependent. In general, the normal PR intervals are 70 to 170 milliseconds in newborns and 80 to 220 milliseconds in young children and adults [41].

Although first-degree AV block does not cause bradycardia, it is important to distinguish this finding from other forms of AV nodal dysfunction.

First-degree AV block is a common ECG finding, which reportedly occurs in up to 6 percent of normal neonates [42]. Although the conduction time from the sinus node to the ventricles is increased, bradycardia does not occur, since AV conduction remains intact. There is an association with sinus node dysfunction or AV node disease in affected patients.

Increased vagal tone is a common and usually benign finding that may result in first-degree AV block. (See 'Hypervagotonia' above.)

Medical conditions associated with first-degree AV block include [43]:

Rheumatic fever

Lyme disease

Chagas disease

Rubella, mumps

Hypothermia

Metabolic derangements (hypokalemia, hyperkalemia, hypocalcemia, hypercalcemia, hypoglycemia, and hypomagnesemia)

Cardiomyopathy

Children with first-degree AV block are usually asymptomatic. Routine monitoring and/or treatment may be indicated if there is evidence of coexisting sinus or AV node dysfunction. (See 'Sinus node dysfunction' above.)

With extreme PR interval prolongation, some patients may develop pacemaker syndrome (dizziness, fatigue, or chest discomfort) due to atrial contraction against a closed mitral valve or when atrial contraction occurs shortly after ventricular systole with incomplete atrial filling. Pacemaker therapy may be indicated for these patients [16]. (See 'Chronic management' below.)

Additional aspects of clinical manifestations and implications of first-degree AV block at different sites in the conduction system are discussed separately. (See "First-degree atrioventricular block".)

Second-degree atrioventricular block — In second-degree AV block, the organized atrial impulse fails to be conducted to the ventricle in a 1:1 ratio. Second-degree AV block is further divided into two categories:

Mobitz type 1 block — In Mobitz type 1 block (also referred to as Wenckebach block), there is progressive prolongation of the PR interval until a P wave fails to be conducted (waveform 4).

Mobitz type 1 block is commonly seen in normal children and young adults, especially at times of high parasympathetic tone (eg, sleep or in well-trained athletes) [44,45]. In one study, Mobitz type 1 block was seen in 6 percent of medical students during sleep [44].

Patients with Mobitz type 1 block are generally asymptomatic. The block is located at the level of the AV node and is usually not associated with other significant conduction system disease. In addition, it does not progress to complete block.

It may also be seen in patients with intrinsic AV nodal disease, myocarditis (including Chagas disease), Lyme disease, or myocardial infarction or following cardiac surgery. These conditions may be associated with other conduction abnormalities.

Treatment is usually not indicated unless there is evidence for other more significant conduction system disease. (See "Second-degree atrioventricular block: Mobitz type I (Wenckebach block)" and 'Acute management of patients with poor perfusion' below.)

Mobitz type 2 block — In Mobitz type 2 block, the PR interval remains unchanged prior to the P wave that suddenly fails to conduct to the ventricles (waveform 5).

Mobitz type 2 block occurs much less frequently than type 1, but its presence has more significant clinical implications [45]. It is associated with various forms of CHD and is seen after cardiac surgery. Type 2 block is thought to occur at or below the level of the AV node, indicating disease within the His bundle and bundle branches. It has a less predictable course and may progress to complete heart block. (See 'Third-degree atrioventricular block' below.)

Advanced second-degree atrioventricular block — Advanced second-degree AV block is diagnosed on ECG when there are two consecutive P waves present that should, but fail to, conduct to the ventricle. This indicates significant conduction disease below the level of the AV node.

Third-degree atrioventricular block — In third-degree AV block, also referred to as complete heart block, there is complete dissociation of the atrial and ventricular activity. The atrial rate (P wave) is greater than the ventricular rate (QRS complex), which is junctional or ventricular in origin (waveform 6).

Complete heart block is further divided into congenital and acquired causes:

Congenital complete heart block — Neonatal lupus, due to maternal antibodies (RO-SSA and LA-SSB) that cross the placenta, is responsible for 60 to 90 percent of congenital complete heart block cases. Other causes include myocarditis and various structural cardiac defects, particularly L-transposition of the great arteries, AV discordance, or polysplenia with AV canal defect. The clinical manifestations, presentation, and treatment of congenital complete heart block are discussed separately. (See "Congenital third-degree (complete) atrioventricular block" and "Neonatal lupus: Epidemiology, pathogenesis, clinical manifestations, and diagnosis".)

Familial AV conduction block, characterized by a progression in the degree of block in association with a variable apparent site of block, may be transmitted as an autosomal dominant trait. (See "Etiology of atrioventricular block", section on 'Familial disease'.)

Acquired complete heart block — Causes of acquired heart block include:

Myocarditis

Lyme disease

Acute rheumatic disease

Myocardial infarction

Trauma

Injury from surgery or catheterization

Cardiomyopathy

Patients with complete heart block and structural heart disease are at increased risk for heart failure as their ability to maintain an adequate cardiac output may be compromised from the low heart rate and a possible reduction in stroke volume. These patients are also at increased risk for sudden cardiac death [46]. (See 'Congenital heart disease' below and 'Outcome' below.)

APPROACH TO MANAGEMENT — Management of bradycardia depends on the cause and clinical circumstances. Children who present acutely with poor perfusion or shock require immediate medical management (algorithm 1). In patients with non-life-threatening symptoms, the management depends upon the frequency and severity of symptoms, the specific conduction abnormality, and whether the child has underlying congenital heart disease (CHD). Children with sinus bradycardia who are asymptomatic and otherwise healthy generally do not require any further evaluation or treatment.

Acute management of patients with poor perfusion — Children who have bradycardia with poor perfusion or shock require immediate medical attention.

We agree with the American Heart Association (AHA) guidelines for cardiopulmonary resuscitation (CPR) for children with bradycardia and poor perfusion, which include the following steps (algorithm 1) [47]:

Assess the airway and circulatory system. Provide airway management, oxygenation, and ventilation as needed. (See "Technique of emergency endotracheal intubation in children" and "Assessment of systemic perfusion in children".)

Begin chest compressions for heart rate <60 beats per minute (bpm) despite adequate ventilation and oxygenation. (See "Pediatric basic life support (BLS) for health care providers", section on 'Chest compressions'.)

Administer a medication to increase the heart rate:

Epinephrine for patients without increased vagal tone or primary atrioventricular (AV) block – Administer epinephrine at a dose of 0.01 mg/kg (0.1 mL/kg of the 0.1 mg/mL concentration) intravenously (IV) or intraosseously (IO). The dose may be repeated every three to five minutes at the same dose. The maximum single dose is 1 mg. (See "Primary drugs in pediatric resuscitation", section on 'Epinephrine'.)

If IV or IO access is not available and the patient is intubated, epinephrine can be administered through the endotracheal tube using a higher dose of 0.1 mg per kg (concentration 1:1000; 0.1 mL per kg of the 1 mg/mL concentration).

Atropine for patients with increased vagal tone or primary AV block – Administer atropine at a dose of 0.02 mg/kg IV or IO (minimum dose 0.1 mg, maximum dose 0.5 mg). The dose may be repeated once. (See "Primary drugs in pediatric resuscitation", section on 'Atropine'.)

Identify and treat potential reversible causes of refractory bradycardia, including hypoxemia, hypothermia, head injury, toxins, and hypervagotonia.

If bradycardia persists, consider cardiac pacing, particularly if a conduction defect is detected or suspected. Cardiac pacing requires that appropriately trained personnel and equipment are available.

Additional principles of pediatric advanced life support are discussed separately. (See "Pediatric advanced life support (PALS)".)

In a registry study of nearly 2800 hospitalized pediatric patients who received CPR for bradycardia with poor perfusion, 31 percent became pulseless after CPR was started (median time to loss of pulses was three minutes) [48]. Children who became pulseless were more likely to have metabolic abnormalities, septicemia, malignancy, or other organ system dysfunction (hypotension, heart failure, renal insufficiency) at the time of the arrest. The duration of CPR was considerably longer for children who became pulseless during the resuscitation (20 versus 4 minutes) and the likelihood of surviving to hospital discharge was lower (30 versus 70 percent). These findings highlight the importance of prompt recognition and treatment of underlying reversible causes of bradycardia with poor perfusion, as well as prompt initiation of good quality CPR followed by appropriate post-resuscitation care. (See "Pediatric advanced life support (PALS)", section on 'Early post-cardiac arrest management' and "Initial post-cardiac arrest care in children", section on 'Approach to stabilization'.)

Chronic management — Management of patients with chronic bradycardia depends on the etiology and degree of symptoms. Permanent pacemaker implantation is the treatment of choice for chronic management of symptomatic bradycardia. Chronic medical therapy is generally not effective, due to variable response over time. In addition, there are unacceptable side effects of chronotropic medications. We generally agree with the recommendations of the Pediatric and Congenital Electrophysiology Society (PACES), American College of Cardiology (ACC), AHA, and Heart Rhythm Society (HRS) regarding indications for permanent pacemaker placement in pediatric patients [16]. (See 'Society guideline links' below.)

A more detailed discussion of indications for permanent pacemaker placement is provided separately. (See "Permanent cardiac pacing: Overview of devices and indications".)

Complete heart block — Definitive treatment of third-degree (complete) AV block generally involves permanent pacemaker placement, as discussed separately. (See "Congenital third-degree (complete) atrioventricular block", section on 'Postnatal treatment' and "Permanent cardiac pacing: Overview of devices and indications", section on 'Acquired AV block'.)

Sinus node dysfunction — The need for permanent pacing in patients with sinus node dysfunction depends upon the correlation of bradycardia with symptoms. For patients with sinus node dysfunction that correlates with symptoms during age- and activity-inappropriate bradycardia, we suggest pacemaker placement [16]. This recommendation is largely extrapolated from the experience in adult patients. There are limited pediatric data to guide management decisions [49]. (See "Permanent cardiac pacing: Overview of devices and indications", section on 'Sinus node dysfunction' and "Sinus node dysfunction: Treatment", section on 'Permanent pacing'.)

Congenital heart disease — Children with underlying CHD who have clinically significant bradycardia may benefit from placement of a permanent pacemaker even in the absence of associated symptoms. The rationale for treatment is based on the concern that bradycardia in these children is associated with heart failure, hemodynamic compromise, and increased risk of sudden cardiac death. (See 'Outcome' below.)

As previously discussed, permanent pacemaker placement is generally warranted for patients with CHD who have acquired third-degree (complete) AV block. (See "Permanent cardiac pacing: Overview of devices and indications", section on 'Acquired AV block' and "Atrial arrhythmias (including AV block) in congenital heart disease", section on 'Permanent pacemaker implantation'.)

In addition, permanent pacemakers are sometimes used in patients with CHD in the following settings, although the evidence to support these indications is less well established [16]:

Sinus bradycardia in patients with complex CHD who have a resting heart rate <40 bpm or prolonged pauses in ventricular rate

Sinus bradycardia associated with recurrent episodes of intra-atrial re-entrant tachycardia when catheter ablation or medication are ineffective or not acceptable treatments

Impaired hemodynamics due to sinus bradycardia or loss of AV synchrony

Sinus node dysfunction, particularly with alternating tachycardia and bradycardia with symptoms attributable to pauses due to sudden-onset bradycardia

Pacemaker implantation for bradyarrhythmias is uncommon following repair of CHD. The frequency depends upon the CHD lesion and the type of repair. (See "Atrial arrhythmias (including AV block) in congenital heart disease".)

The surgeries that are most commonly associated with pacemaker placement include [29,50,51]:

Surgical closure of atrial septal defect (up to 4 percent) (see "Isolated atrial septal defects (ASDs) in children: Management and outcome")

Fontan (7 percent patients) (see "Management of complications in patients with Fontan circulation")

Atrial switch operation (over 80 percent) (see "D-transposition of the great arteries (D-TGA): Management and outcome", section on 'Mustard and Senning procedures')

Asymptomatic bradycardia in otherwise healthy children — No additional evaluation or treatment is needed in children with sinus bradycardia who are asymptomatic and otherwise healthy. Although data are limited, asymptomatic sinus bradycardia in healthy children does not appear to have any prognostic significance. (See 'Outcome' below.)

OUTCOME

Asymptomatic bradycardia in healthy children — Asymptomatic sinus bradycardia in healthy children does not appear to have any prognostic significance.

In a study of 104 adolescents identified with sinus bradycardia through a population-based screening program, 17 percent of the participants had self-limited syncopal episodes, but none had experienced life-threatening events during the 10-year follow-up period [52]. Additional evaluation in a subgroup of patients did not detect any HCN4 gene mutations, which are associated with sinus node dysfunction. (See "Sinus node dysfunction: Epidemiology, etiology, and natural history", section on 'Childhood and familial disease'.)

Bradycardia in children with congenital heart disease — Bradycardia is associated with an increased risk of sudden death in both unoperated and operated patients with congenital heart disease. As an example, the reported incidence of sudden death among patients with sinus node dysfunction following atrial switch operation (Mustard procedure) is 2.5 percent [29]. Although no specific etiology was determined, cardiac arrhythmia was considered the likely cause of death. (See 'Sinus node dysfunction' above and "D-transposition of the great arteries (D-TGA): Management and outcome", section on 'Mustard and Senning procedures'.)

Sinus node dysfunction has been associated with lower physical performance and possible risk for atrial arrhythmias in patients following the Fontan operation. The incidence of sinus node dysfunction has been reported as high as 45 percent. However, a multicenter study found that resting bradycardia was not associated with poor functional outcomes in this population [53].

Complete heart block — The mortality rate in children with untreated complete heart block is 5 to 8 percent [46]. Complete heart block is also associated with development of cardiomyopathy. Patients with complete heart block therefore require serial annual echocardiograms to evaluate and monitor left ventricular size and function. (See "Congenital third-degree (complete) atrioventricular block", section on 'Prognosis'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Arrhythmias in children" and "Society guideline links: Basic and advanced cardiac life support in children".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or email these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient education" and the keyword[s] of interest.)

Basics topics (see "Patient education: Bradycardia (The Basics)" and "Patient education: Heart block in adults (The Basics)" and "Patient education: Heart block in children (The Basics)")

SUMMARY AND RECOMMENDATIONS

Definition – Bradycardia is defined as a heart rate measured in the awake state that is below the normal range for age (table 1). (See 'Definition' above.)

Causes of bradycardia – Bradycardia may be caused by intrinsic dysfunction or injury to the heart's conduction system or by extrinsic factors acting on a normal heart and its conduction system (table 2). The most common causes in children include increased vagal tone, medications (table 3), and corrective surgery of congenital heart disease (CHD). (See 'Definition' above and 'Causes of bradycardia' above.)

Clinical presentation

Unstable patients – If cardiac output is insufficient, the patient may present with poor systemic perfusion or cardiorespiratory arrest. Patients with severe bradycardia and poor perfusion require immediate cardiopulmonary resuscitation as summarized in the algorithm (algorithm 1). (See 'Acute management of patients with poor perfusion' above and "Pediatric advanced life support (PALS)".)

Stable patients – Most children with bradycardia are asymptomatic. In infants and preverbal children, symptoms, when present, may be nonspecific, including lethargy, poor feeding, and/or seizures. Older children and adolescents may complain of dizziness, fatigue, exercise intolerance, and/or syncope. (See 'Clinical presentation' above.)

Evaluation – In the stable patient with bradycardia, evaluation includes a medical history, physical examination, and electrocardiogram (ECG). Additional studies that may be useful include ambulatory ECG monitoring (eg, Holter monitor or other wearable device), echocardiogram, exercise stress testing, and, rarely, invasive electrophysiology testing. (See 'Evaluation' above.)

Based upon the ECG findings, the type of rhythm abnormality can be determined (see 'Identifying the type of rhythm abnormality' above):

Sinus bradycardia – Asymptomatic sinus bradycardia (waveform 1) is a common finding in healthy children. No additional evaluation or treatment is needed in children with sinus bradycardia who are asymptomatic and otherwise healthy. Increased vagal tone can cause sinus bradycardia that may be symptomatic. (See 'Sinus bradycardia' above and 'Hypervagotonia' above.)

Sinus node dysfunction – Sinus node dysfunction (waveform 2), defined as inappropriate sinus bradycardia or inability to appropriately elevate the heart rate in response to physiologic stress, can be caused by congenital, familial, or cardiac disease. It can also be acquired from direct injury (surgery), inflammation (myocarditis), or medications. (See 'Sinus node dysfunction' above.)

First-degree (atrioventricular) AV block – First-degree AV block (slowed conduction without missed beats (waveform 3)) is frequently observed in healthy asymptomatic children and does not cause bradycardia. (See 'First-degree atrioventricular block' above.)

Second-degree AV block – Second-degree AV block (intermittent conduction with missed beats) includes Mobitz types 1 (waveform 4) and 2 (waveform 5). Patients with Mobitz type 1 block are generally asymptomatic. Children with Mobitz type 2 block are more likely to have underlying cardiac disease and are at increased risk to progress to complete heart block. (See 'Second-degree atrioventricular block' above.)

Complete AV block – Third-degree or complete heart block (absent conduction (waveform 6)) can be congenital or acquired. In the neonate, the most common cause is neonatal lupus. (See 'Third-degree atrioventricular block' above.)

Management

Acute management – Unstable patients presenting with severe bradycardia require immediate cardiopulmonary resuscitation as summarized in the algorithm (algorithm 1). Initial interventions aim to identify and address reversible causes of bradycardia (eg, hypoxemia). Epinephrine and/or atropine may be required if bradycardia persists despite assisted ventilation. (See 'Acute management of patients with poor perfusion' above and "Pediatric advanced life support (PALS)".)

Chronic management – Management of patients with chronic bradycardia depends on the etiology and degree of symptoms. (See 'Chronic management' above.)

In patients who require intervention, pacemaker implantation is the treatment of choice for chronic management symptomatic bradycardia. Indications for permanent pacemaker placement are discussed separately. (See "Permanent cardiac pacing: Overview of devices and indications".)

ACKNOWLEDGMENT — The editorial staff at UpToDate acknowledge Frank Zimmerman, MD, who contributed to an earlier version of this topic review.

  1. Fleming S, Thompson M, Stevens R, et al. Normal ranges of heart rate and respiratory rate in children from birth to 18 years of age: a systematic review of observational studies. Lancet 2011; 377:1011.
  2. Davignon A. ECG standards for children. Pediatr Cardiol 1980; 1:133.
  3. Rijnbeek PR, Witsenburg M, Schrama E, et al. New normal limits for the paediatric electrocardiogram. Eur Heart J 2001; 22:702.
  4. Saarel EV, Granger S, Kaltman JR, et al. Electrocardiograms in Healthy North American Children in the Digital Age. Circ Arrhythm Electrophysiol 2018; 11:e005808.
  5. Kugler JD. Sinus node dysfunction. In: Pediatric Arrhythmias: Electrophysiology and Pacing, Gillette PC, Garson AG Jr (Eds), WB Saunders, Philadelphia 1990. p.250.
  6. Richards JM, Alexander JR, Shinebourne EA, et al. Sequential 22-hour profiles of breathing patterns and heart rate in 110 full-term infants during their first 6 months of life. Pediatrics 1984; 74:763.
  7. Southall DP, Johnston F, Shinebourne EA, Johnston PG. 24-hour electrocardiographic study of heart rate and rhythm patterns in population of healthy children. Br Heart J 1981; 45:281.
  8. Montague TJ, Taylor PG, Stockton R, et al. The spectrum of cardiac rate and rhythm in normal newborns. Pediatr Cardiol 1982; 2:33.
  9. Mangrum JM, DiMarco JP. The evaluation and management of bradycardia. N Engl J Med 2000; 342:703.
  10. Recognition and management of bradycardia. In: Pediatric Advanced Life Support Provider Manual, Chameides L, et al (Eds), American Heart Association, Dallas 2011. p.113.
  11. Yabek SM, Jarmakani JM. Sinus node dysfunction in children, adolescents, and young adults. Pediatrics 1978; 61:593.
  12. Rein AJ, Simcha A, Ludomirsky A, et al. Symptomatic sinus bradycardia in infants with structurally normal hearts. J Pediatr 1985; 107:724.
  13. Bricker JT, Garson A Jr, Gillette PC. A family history of seizures associated with sudden cardiac deaths. Am J Dis Child 1984; 138:866.
  14. Beder SD, Cohen MH, Riemenschneider TA. Occult arrhythmias as the etiology of unexplained syncope in children with structurally normal hearts. Am Heart J 1985; 109:309.
  15. Bolourchi M, Batra AS. Diagnostic yield of patch ambulatory electrocardiogram monitoring in children (from a national registry). Am J Cardiol 2015; 115:630.
  16. Writing Committee Members, Shah MJ, Silka MJ, et al. 2021 PACES Expert Consensus Statement on the Indications and Management of Cardiovascular Implantable Electronic Devices in Pediatric Patients: Developed in collaboration with and endorsed by the Heart Rhythm Society (HRS), the American College of Cardiology (ACC), the American Heart Association (AHA), and the Association for European Paediatric and Congenital Cardiology (AEPC) Endorsed by the Asia Pacific Heart Rhythm Society (APHRS), the Indian Heart Rhythm Society (IHRS), and the Latin American Heart Rhythm Society (LAHRS). JACC Clin Electrophysiol 2021; 7:1437.
  17. Gropler MRF, Dalal AS, Van Hare GF, Silva JNA. Can smartphone wireless ECGs be used to accurately assess ECG intervals in pediatrics? A comparison of mobile health monitoring to standard 12-lead ECG. PLoS One 2018; 13:e0204403.
  18. Turakhia MP, Desai M, Hedlin H, et al. Rationale and design of a large-scale, app-based study to identify cardiac arrhythmias using a smartwatch: The Apple Heart Study. Am Heart J 2019; 207:66.
  19. Campbell RM, Douglas PS, Eidem BW, et al. ACC/AAP/AHA/ASE/HRS/SCAI/SCCT/SCMR/SOPE 2014 appropriate use criteria for initial transthoracic echocardiography in outpatient pediatric cardiology: a report of the American College of Cardiology Appropriate Use Criteria Task Force, American Academy of Pediatrics, American Heart Association, American Society of Echocardiography, Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular Computed Tomography, Society for Cardiovascular Magnetic Resonance, and Society of Pediatric Echocardiography. J Am Coll Cardiol 2014; 64:2039.
  20. Guidelines for Clinical Intracardiac Electrophysiological and Catheter Ablation Procedures. A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines. (Committee on Clinical Intracardiac Electrophysiologic and Catheter Ablation Procedures). Developed in collaboration with the North American Society of Pacing and Electrophysiology. Circulation 1995; 92:673.
  21. Lombroso CT, Lerman P. Breathholding spells (cyanotic and pallid infantile syncope). Pediatrics 1967; 39:563.
  22. Stephenson JB. Reflex anoxic seizures ('white breath-holding'): nonepileptic vagal attacks. Arch Dis Child 1978; 53:193.
  23. Di Fiore J, Arko M, Herynk B, et al. Characterization of cardiorespiratory events following gastroesophageal reflux in preterm infants. J Perinatol 2010; 30:683.
  24. Bateman BT, Patorno E, Desai RJ, et al. Late Pregnancy β Blocker Exposure and Risks of Neonatal Hypoglycemia and Bradycardia. Pediatrics 2016; 138.
  25. Swiryn S, McDonough T, Hueter DC. Sinus node function and dysfunction. Med Clin North Am 1984; 68:935.
  26. Ruschhaupt DG, Khoury L, Thilenius OG, et al. Electrophysiologic abnormalities of children with ostium secundum atrial septal defect. Am J Cardiol 1984; 53:1643.
  27. Bolens M, Friedli B. Sinus node function and conduction system before and after surgery for secundum atrial septal defect: an electrophysiologic study. Am J Cardiol 1984; 53:1415.
  28. Fournier A, Young ML, Garcia OL, et al. Electrophysiologic cardiac function before and after surgery in children with atrioventricular canal. Am J Cardiol 1986; 57:1137.
  29. Flinn CJ, Wolff GS, Dick M 2nd, et al. Cardiac rhythm after the Mustard operation for complete transposition of the great arteries. N Engl J Med 1984; 310:1635.
  30. Duster MC, Bink-Boelkens MT, Wampler D, et al. Long-term follow-up of dysrhythmias following the Mustard procedure. Am Heart J 1985; 109:1323.
  31. Kavey RE, Gaum WE, Byrum CJ, et al. Loss of sinus rhythm after total cavopulmonary connection. Circulation 1995; 92:II304.
  32. Mehta AV, Chidambaram B, Garrett A. Familial symptomatic sinus bradycardia: autosomal dominant inheritance. Pediatr Cardiol 1995; 16:231.
  33. Nordenberg A, Varghese PJ, Nugent EW. Spectrum of sinus node dysfunction in two siblings. Am Heart J 1976; 91:507.
  34. Lehmann H, Klein UE. Familial sinus node dysfunction with autosomal dominant inheritance. Br Heart J 1978; 40:1314.
  35. Ward DE, Ho SY, Shinebourne EA. Familial atrial standstill and inexcitability in childhood. Am J Cardiol 1984; 53:965.
  36. Benson DW, Wang DW, Dyment M, et al. Congenital sick sinus syndrome caused by recessive mutations in the cardiac sodium channel gene (SCN5A). J Clin Invest 2003; 112:1019.
  37. Bini RM, Westaby S, Bargeron LM Jr, et al. Investigation and management of primary cardiac tumors in infants and children. J Am Coll Cardiol 1983; 2:351.
  38. Miller KK, Grinspoon SK, Ciampa J, et al. Medical findings in outpatients with anorexia nervosa. Arch Intern Med 2005; 165:561.
  39. Brucato A, Previtali E, Ramoni V, Ghidoni S. Arrhythmias presenting in neonatal lupus. Scand J Immunol 2010; 72:198.
  40. Baird TM. Clinical correlates, natural history and outcome of neonatal apnoea. Semin Neonatol 2004; 9:205.
  41. Garson A Jr. Arrhythmias. In: The Electrocardiogram in Infants and Children: A Systematic Approach, Lea & Febiger, Philadelphia 1983. p.195.
  42. Ferrer PL. Arrhythmias in the neonate. In: Arrhythmias in the neonate, infant, and child, Roberts NK, Gleband H (Eds), Appleton-Century-Crofts, New York 1977. p.265.
  43. Ross BA, Trippel DL. Atrioventricular block. In: The science and practice of pediatric cardiology, Garson A, Bricker JT, Fisher DJ, Neish SR (Eds), Willilmans & Wilkins, Philadelphia 1998. p.2048.
  44. Brodsky M, Wu D, Denes P, et al. Arrhythmias documented by 24 hour continuous electrocardiographic monitoring in 50 male medical students without apparent heart disease. Am J Cardiol 1977; 39:390.
  45. Dickinson DF, Scott O. Ambulatory electrocardiographic monitoring in 100 healthy teenage boys. Br Heart J 1984; 51:179.
  46. Michaelson M, Engle MA. Congenital complete heart block: An international study of the natural history. In: Cardiovascular Clinics, Brest AN, Engle MA (Eds), FA Davis, Philadelphia 1972. p.85.
  47. Kleinman ME, Chameides L, Schexnayder SM, et al. Part 14: pediatric advanced life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010; 122:S876.
  48. Khera R, Tang Y, Girotra S, et al. Pulselessness After Initiation of Cardiopulmonary Resuscitation for Bradycardia in Hospitalized Children. Circulation 2019; 140:370.
  49. Albin G, Hayes DL, Holmes DR Jr. Sinus node dysfunction in pediatric and young adult patients: treatment by implantation of a permanent pacemaker in 39 cases. Mayo Clin Proc 1985; 60:667.
  50. Allen MR, Hayes DL, Warnes CA, Danielson GK. Permanent pacing in Ebstein's anomaly. Pacing Clin Electrophysiol 1997; 20:1243.
  51. Cohen MI, Wernovsky G, Vetter VL, et al. Sinus node function after a systematically staged Fontan procedure. Circulation 1998; 98:II352.
  52. Chiu SN, Lin LY, Wang JK, et al. Long-term outcomes of pediatric sinus bradycardia. J Pediatr 2013; 163:885.
  53. Blaufox AD, Sleeper LA, Bradley DJ, et al. Functional status, heart rate, and rhythm abnormalities in 521 Fontan patients 6 to 18 years of age. J Thorac Cardiovasc Surg 2008; 136:100.
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References

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