Approach to the child with tachycardia

INTRODUCTION — Tachycardia is common in the pediatric age group, and the etiology is often benign. A parent/caregiver or other observer may describe tachycardia based on observation of the child's neck veins, palpation of the pulse, or sensation of the heart beating rapidly while holding the child. All complaints of tachycardia require rapid assessment of patient status and cardiac rhythm. In most instances, life-threatening tachycardia can be rapidly detected and treated. This topic will review the differential diagnosis and approach to the child who presents with tachycardia.

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of tachycardia in children is provided in the table (table 1).

Life-threatening cardiac conditions — Most life-threatening cardiac conditions in children that present as tachycardia consist of supraventricular tachycardias. However, any type of arrhythmia may occur depending on specific patient predisposition [1].

●Supraventricular tachycardia (SVT) – While the term "SVT" technically includes the entire group of tachycardias whose mechanisms involve the atria and/or atrioventricular (AV) node, in common parlance the term also describes the most common pathologic supraventricular tachycardia in children: tachycardia caused by an accessory AV pathway (eg, AV reentrant tachycardia). The dual use of this term can lead to confusion when communicating among team members and consultants.

SVT may present with palpitations, chest pain, or shortness of breath in children, or with lethargy, feeding difficulties, or irritability in infants. In many instances, a parent/caregiver or health care provider notes a rapid heart rate during routine care. In newborns and infants with SVT, the heart rate is typically >220 beats per minute (BPM), while in older children the heart rate is >180 BPM [2].

Children may exhibit a range of clinical findings, from no symptoms to cardiogenic shock, depending on the duration of SVT.

The term Wolff-Parkinson-White syndrome (WPW) is applied when there is a shortened PR interval and ventricular pre-excitation on the resting electrocardiogram (ECG) due to the accessory pathway. If the accessory pathway is not apparent on resting ECG, the pathway is considered "concealed". SVT may also be associated with drug exposure, especially sympathomimetics contained in high caffeine drinks, cough/cold medications, short-acting beta agonists, and dietary supplements, or congenital heart disease (eg, Ebstein anomaly, repaired dextrotransposition of the great arteries, single ventricle lesions after Fontan operation). (See "Approach to the child with occult toxic exposure" and "Clinical features and diagnosis of supraventricular tachycardia (SVT) in children".)

●Ventricular tachycardia (VT) – This arrhythmia is uncommon in the pediatric population. VT may result from electrolyte abnormalities (hyperkalemia, hypocalcemia, and hypomagnesemia), congenital heart disorders, myocarditis, myocardial ischemia caused by congenital abnormality of the coronary arteries, or drug toxicity. In addition, patients who have undergone cardiac surgery (eg, ventriculotomy for repair of tetralogy of Fallot) are at risk for these dysrhythmias due to postoperative ventricular scarring [3]. (See "Causes of wide QRS complex tachycardia in children".)

●Torsades de Pointes (TdP) – TdP, or polymorphous ventricular tachycardia, is the hallmark dysrhythmia associated with long QT syndrome (LQTS). LQTS may be hereditary (Jervell-Lange-Nielsen syndrome or Romano-Ward syndrome) or acquired [4]. Acquired TdP may follow hypokalemia, hypocalcemia, hypomagnesemia, and ingestion of drugs with sodium channel or inwardly rectifying potassium channel blocking properties, such as cyclic antidepressants and certain antiarrhythmic medications (table 2). TdP has the potential to rapidly deteriorate into ventricular fibrillation and sudden death [5]. (See "Congenital long QT syndrome: Epidemiology and clinical manifestations" and "Acquired long QT syndrome: Definitions, pathophysiology, and causes".)

●Atrial flutter – Atrial flutter is a supraventricular tachycardia that is caused by an intraatrial reentry circuit. Most children with atrial flutter have an underlying heart abnormality, such as repaired or palliated congenital heart disease. Though most patients with atrial flutter are hemodynamically stable, there is a risk of sudden death if this dysrhythmia cannot be medically or surgically controlled [6].

●Hypertrophic cardiomyopathy (HCM) – HCM manifests as a hypertrophied, nondilated left ventricle and septum. Patients with HCM may present with palpitations, syncope, or cardiac arrest during strenuous exercise. Tachycardias in these patients can be either supraventricular, including sinus tachycardia, or ventricular. The subset of HCM patients who present with syncope are at significant risk for sudden death [7]. (See "Hypertrophic cardiomyopathy in children: Clinical manifestations and diagnosis".)

●Myocarditis – This inflammation of the myocardium is most commonly viral in origin, with Coxsackie virus B and other enteroviruses accounting for most cases. Clinical findings of myocarditis include tachycardia, typically sinus or ventricular, out of proportion to fever or at rest, poor perfusion, and signs of heart failure. Patients with myocarditis may progress rapidly to cardiogenic shock [8]. (See "Clinical manifestations and diagnosis of myocarditis in children".)

●Pericardial effusion with cardiac tamponade – This condition may occur in patients with infectious pericarditis, blunt chest trauma, or as a component of post-pericardiotomy syndrome in patients with fever and large pericardial effusion following recent heart surgery. Sinus tachycardia is seen in almost all patients, allowing for at least partial maintenance of cardiac output. (See "Pericardial effusion: Approach to diagnosis".)

Life-threatening noncardiac conditions

●Substrate deficiency – Oxygen and glucose are key physiologic substrates. Both hypoxemia and hypoglycemia are important causes of sinus tachycardia and are life-threatening if not immediately recognized and treated.

●Hypovolemic shock – Inadequate perfusion of tissues caused by hemorrhage or extravascular fluid loss results in sinus tachycardia with vasoconstriction and a narrowed pulse pressure. (See "Hypovolemic shock in children in resource-abundant settings: Initial evaluation and management".)

●Electrolyte imbalance – Hyperkalemia and hypocalcemia are caused by a variety of conditions and are associated with atrial and ventricular tachyarrhythmias. (See "Causes and evaluation of hyperkalemia in adults" and "Diagnostic approach to hypocalcemia".)

●Sepsis – Sinus tachycardia may be an early and persistent sign of obvious or occult sepsis and accompanies septic shock. (See "Sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis".)

●Anaphylaxis – Anaphylaxis is usually characterized by a defined exposure to a potential trigger, followed by rapid onset, evolution, and resolution of cutaneous, respiratory, cardiovascular, and/or gastrointestinal symptoms within minutes to hours. (See "Anaphylaxis: Emergency treatment".)

●Toxic exposure – Many toxic exposures have the potential to cause life-threatening tachyarrhythmias. The specific arrhythmia depends on the characteristics of the toxic agent (table 2).

Common conditions — Sinus tachycardia may result from exercise, fever, anemia, drugs (especially caffeine), anxiety/hyperventilation syndrome, emotional arousal, and pain (table 1).

Other conditions

●Acute rheumatic fever – Acute rheumatic fever (ARF) is a delayed, nonsuppurative sequela of a pharyngeal infection with the group A streptococcus. Fever and pancarditis are clinical manifestations of this disease that can rarely cause tachydysrhythmias [9]. Other findings include arthralgia, arthritis, erythema marginatum, subcutaneous nodules, and chorea. Testing for recent streptococcal infection is essential to establish the diagnosis. (See "Acute rheumatic fever: Clinical manifestations and diagnosis".)

●Hyperthyroidism – Patients with hyperthyroidism have an increase in cardiac output, caused by both increased peripheral oxygen needs and increased cardiac contractility. Heart rate is increased, pulse pressure is widened, and peripheral vascular resistance is decreased [10]. Atrial fibrillation, which occurs in 10 to 20 percent of adults with hyperthyroidism, is rare in children. Mitral valve prolapse is two to three times more prevalent in hyperthyroid patients than in normal subjects [11]. (See "Clinical manifestations and diagnosis of Graves disease in children and adolescents".)

●Kawasaki disease – Kawasaki disease is a systemic inflammation that typically presents with fever and irritability. Other diagnostic criteria include bilateral nonexudative conjunctivitis, erythema of the lips and oral mucosa, rash, extremity changes, and lymphadenopathy. Tachycardia accompanies fever and may also signify serious cardiac effects such as pericardial effusion, heart failure, and coronary artery aneurysm. (See "Kawasaki disease: Clinical features and diagnosis".)

●Pheochromocytoma – Pheochromocytomas and paragangliomas are rare neoplasms in children. Tumors that arise from the adrenal medulla are termed pheochromocytomas, and those with extraadrenal origins are called paragangliomas. The classic triad of symptoms in these disorders consists of episodic headache, sweating, and tachycardia, usually accompanied by hypertension. Malignant hypertension can occur, with its associated complications (eg, increased intracranial pressure, encephalopathy). (See "Pheochromocytoma and paraganglioma in children" and "Moderate to severe hypertensive retinopathy and hypertensive encephalopathy in adults".)

EVALUATION

History — A thorough history can help the clinician delineate the cause of tachycardia.

●Feeding difficulty with tachypnea – Infants with heart failure may present with a history of sweating with feeds, feeding difficulty and tachypnea, or agitation.

●Precipitating factors – Fever, anemia, and exercise are common causes of sinus tachycardia.

●Emotional state – The patient's emotional state before the onset of tachycardia should be discussed to determine the likelihood of anxiety as the cause of symptoms.

●Recent medications, intoxication, drug, and caffeine use – Sympathomimetic medications may be a trigger for tachycardia and/or arrhythmias, such as cough or cold preparations (see "Over-the-counter cough and cold preparations: Approach to pediatric poisoning", section on 'Phenylephrine and similar decongestants'), beta-agonists, toxic exposures, drugs of abuse, unregulated dietary substances such as ephedra, caffeine-containing beverages, and weight-loss supplements (table 2). (See "Approach to the child with occult toxic exposure".)

●Illness/fever – A history of viral illness or fever in conjunction with respiratory distress or myocardial dysfunction suggests myocarditis, especially if tachycardia is out of proportion to the degree of fever or is present after defervescence. (See "Clinical manifestations and diagnosis of myocarditis in children".)

A history of a recent streptococcal infection in the febrile patient with tachycardia raises clinical suspicion for acute rheumatic fever. If signs of carditis, such as a murmur of mitral valve regurgitation or pericardial rub are present, then the patient meets Jones criteria for the diagnosis of acute rheumatic fever. (See "Acute rheumatic fever: Clinical manifestations and diagnosis".)

●Heart disease/heart surgery – A history of heart disease or heart surgery increases the risk of secondary atrial and ventricular tachyarrhythmias and post-pericardiotomy syndrome.

●Family history – Family history of sudden cardiac death or deafness may raise clinical suspicion for genetic disorders such as long QT syndrome and hypertrophic cardiomyopathy that may cause sudden onset of ventricular tachycardia.

Physical examination — The patient's hemodynamic status drives decision making for the tachycardic patient. Therefore, the initial general assessment of hemodynamic stability is of paramount importance when evaluating a patient with tachycardia. Clinicians should emergently treat the patient with cardiovascular collapse per American Heart Association guidelines for cardiopulmonary resuscitation (algorithm 1) [2].

Vital signs — Tachycardia is defined as the presence of a heart rate value greater than expected for age. Although values are published for specific age groups (table 3), clinicians may use the basic guideline of >160 BPM for infants (<2 years), >140 BPM for children (2 to 12 years), and >100 BPM for adolescents and adults to define tachycardia (table 4). Oxygen desaturation may be present in patients with unrepaired or palliated congenital heart disease.

Fever suggests the presence of infection and is most commonly associated with sinus tachycardia although the stress of infection may also precipitate many dysrhythmias.

In febrile children with sinus tachycardia, the heart rate increase attributable to elevated temperature may be adjusted by deducting approximately 10 beats/minute for every 1°C elevation in temperatures above 37°C [12-14]. This correction may be of diagnostic benefit when determining the etiology of tachycardia. However, if fever is felt to be the cause of tachycardia, then the elevated heart rate should resolve when the temperature returns to normal.

Cardiovascular findings — Rate irregularity, if present, should be noted. Distant-sounding heart tones may be present in pericardial effusion with tamponade along with pulsus paradoxus. Third and fourth heart sounds or gallop rhythm suggest the presence of myocardial dysfunction. The presence of a murmur suggests underlying structural heart disease. However, innocent "flow" murmurs may be accentuated by hyperdynamic states such as fever, anemia, and sepsis. A laterally displaced point of maximum Impulse (PMI) suggests the presence of cardiomegaly. (See "Pulsus paradoxus in pericardial disease" and "Irregular heart rhythm (arrhythmias) in children" and "Approach to the infant or child with a cardiac murmur".)

Non-cardiovascular findings — Dry-appearing or "tacky" mucous membranes suggest dehydration/hypovolemia. Pallor is seen with anemia. Tachypnea, rales, and hepatomegaly are signs of heart failure. Poor perfusion with bounding pulses suggests the "warm shock" of sepsis. Headache and diaphoresis are associated with pheochromocytoma. A widened pulse pressure and thyromegaly may indicate hyperthyroidism.

Ancillary studies — In the acutely symptomatic patient with tachycardia, monitoring and assessment of the cardiac rhythm and blood pressure is vital. Bedside cardiac monitors often do not provide satisfactory rhythm tracings to permit detailed decision making. Thus, a standard 12-lead ECG and rhythm strip should be obtained upon presentation and concurrent with any attempts at cardioversion or defibrillation to guide therapy and provide valuable data should the patient require pediatric cardiology consultation [15]. Even in the asymptomatic patient, continuous monitoring and a standard ECG is often helpful since an ECG is essential in the diagnosis of WPW and long QT syndrome and may be helpful in the diagnosis of premature atrial and ventricular complexes.

Clinicians should evaluate the presence of electrolyte abnormalities by performing rapid determinations of serum electrolytes, glucose, and calcium. Readily available hemoglobin/hematocrit point of care testing can confirm clinical suspicion of anemia.

Patients with sepsis warrant measurement of a complete blood count with differential and detection of the causative organism through appropriate cultures of the blood, urine, and cerebrospinal fluid. In addition, wound cultures and nasopharyngeal swabs for Staphylococcus aureus are important adjuncts for detection of toxic shock and toxic streptococcal syndromes. (See "Approach to the ill-appearing infant (younger than 90 days of age)".)

Clinical findings suggestive of hyperthyroidism can be confirmed by serum thyroid testing. Serum levels of thyroxine (T4) and triiodothyronine (T3) are elevated, and TSH secretion is suppressed in hyperthyroidism. (See "Clinical manifestations and diagnosis of Graves disease in children and adolescents".)

If the patient presents with an acute tachydysrhythmia, the clinician should obtain an echocardiogram to evaluate myocardial function, as well as to evaluate for underlying structural heart disease soon after normal sinus rhythm is established. In the hemodynamically unstable patient, this study should be performed on an emergent basis, as the information will affect therapeutic decision making. Given its availability in most clinical settings, it is reasonable to get a screening chest radiograph to look for cardiomegaly as supportive data to proceed with cardiology consultation and echocardiogram. (See "Suspected heart disease in infants and children: Criteria for referral", section on 'Timing of referral'.)

Cardiac troponin levels (troponin-I and -T) may be elevated in myocarditis. However, myocardial enzymes (creatine kinase [CK], MB isoenzyme of CK [CK-MB]) levels are generally not helpful as they are rarely abnormal [8]. Serum PCR identification of a viral infection, or viral isolation from other body sites, such as the oropharynx or gastrointestinal tract, can support the diagnosis.

Antistreptolysin O (ASO), anti-deoxyribonuclease B (anti-DNase B), and antihyaluronidase titers are essential for documenting antecedent streptococcal infection as part of the diagnosis of rheumatic fever [16].

ALGORITHMIC APPROACH — The majority of previously healthy pediatrics patients presenting with tachycardia have a febrile illness, mild to moderate dehydration, or anxiety. Ascertainment of a history of known cardiac disease, assessment for shock, and the determination of rhythm are three key decision points in the evaluation of children with tachycardia (algorithm 2). Cardiac arrhythmias, other than sinus tachycardia, are rare in children. A past medical history of congenital heart disease, cardiac surgery, or a family history of sudden death significantly increases the likelihood of life-threatening atrial and ventricular arrhythmias.

Shock — The child with tachycardia and shock should be triaged and managed per the American Heart Association (AHA) guidelines for assessment of cardiopulmonary instability espoused in the Pediatric Advanced Life Support (PALS) course [2]. A key component of this assessment requires categorization of the QRS complex from the cardiorespiratory (CR) monitor or 12-lead ECG as narrow or wide (algorithm 1) [2,17]. A 12-lead ECG before, during, and after intervention is preferable if patient status allows.

●Wide complex tachycardia – Hemodynamically unstable patients with wide complex tachycardia most commonly have VT or SVT with aberrancy (eg, a rate-related bundle branch block where differential properties for impulse conduction between the bundles of His lead to a wide QRS complex despite a supraventricular mechanism). Although there are exceptions, a patient with wide QRS complex tachycardia should be considered to have ventricular tachycardia until an alternative diagnosis can be confirmed. Hyperkalemia, hypocalcemia, hypomagnesemia, or toxic exposures are important etiologies of unstable VT that require specific therapy beyond AHA guidelines for successful rhythm termination (algorithm 1). Type 1a and 1c antiarrhythmic agents (eg, procainamide, flecainide) are contraindicated in patients with drug induced ventricular tachycardia. (See "Management and evaluation of wide QRS complex tachycardia in children".)

Patients with Torsades de Pointes should receive intravenous magnesium sulfate if initial cardioversion is unsuccessful. (See "Acquired long QT syndrome: Clinical manifestations, diagnosis, and management", section on 'Patients with acute TdP'.)

●Narrow complex tachycardia – In a child with a narrow complex arrhythmia, clinicians should classify the patient's rhythm as "sinus" or "non-sinus" by identifying the morphology and timing of the P waves.

●Supraventricular tachycardia (SVT) – Approximately 90 percent of pediatric patients who have non-sinus, narrow complex tachycardia will have atrioventricular reentrant (typical) supraventricular tachycardia [18]. Other patients, especially those with underlying structural heart disease, present with other forms of SVT [19]. Rapid intravenous administration of adenosine may be attempted first if intravenous access is immediately available. Otherwise, unstable patients should receive synchronized cardioversion at 0.5 to 1 J/kg (algorithm 1). Adenosine should be used with extreme caution in patients who have undergone heart transplantation. Denervation of the graft organ may predispose the patient to an extended period of ventricular asystole with standard dose adenosine [20]. (See "Management of supraventricular tachycardia (SVT) in children".)

●Sinus tachycardia – Sinus tachycardia, a nonspecific sign with a wide differential diagnosis, is the most common narrow complex arrhythmia found in children with shock. Initial care must evaluate for substrate deficiency (ie, hypoxemia or hypoglycemia) that is frequently associated with shock. Although the cause of shock may not be initially apparent, treatment must begin immediately. A systematic approach to the evaluation of children with evidence of poor perfusion typically identifies features of the history, physical examination, and ancillary studies that suggest the etiology of the underlying condition (algorithm 3). (See "Initial evaluation of shock in children".)

No shock — Pediatric patients with an acute, ongoing episode of tachycardia may have signs of cardiac disease even though shock is not present (algorithm 4). Typically, there is adequate time to obtain a 12-lead ECG and rhythm strip to categorize the QRS complex as narrow or wide. In addition, a 12 lead ECG obtained prior to and during any therapeutic interventions is essential because the data will allow thorough review of the event by a pediatric cardiologist and will affect long term decision making [21].

Cardiac arrhythmias other than sinus tachycardia are rare in children. A past medical history of congenital heart disease, cardiac surgery, or a family history of sudden death significantly increases the likelihood of life-threatening atrial and ventricular arrhythmias.

●Wide complex tachycardia – In a stable patient with wide QRS complex tachycardia, the goals of the initial evaluation include the following:

•To determine if the wide QRS complex tachycardia originates from the ventricles or is supraventricular with aberrant intraventricular conduction. The treatment and long-term prognosis differs between children with VT versus those with SVT.

•To determine what therapeutic intervention(s) is required acutely.

•After determining the origin of the wide QRS complex tachycardia in the stable patient, treatment can be targeted to the specific arrhythmia. (See "Management and evaluation of wide QRS complex tachycardia in children".)

●Supraventricular tachycardia (SVT) – SVT is characterized by a nonspecific history, absent P waves, no beat-to-beat variability, and a heart rate that is ≥220 beats per minute in infants <1 year of age and ≥180 beats per minute in older children. Stable patients with SVT may initially undergo vagal maneuvers to convert to sinus rhythm. First line medical therapy consists of rapid intravenous infusion of adenosine (0.1 mg/kg) (algorithm 1). If the patient's rhythm cannot be readily determined because the P waves cannot be identified, it is reasonable to give a dose of adenosine while recording a rhythm strip for diagnostic purposes. If the patient does not have a reentrant mechanism, the resultant slowing of the ventricular rate caused by adenosine will often allow for more specific identification of the P wave. (See "Management of supraventricular tachycardia (SVT) in children".)

●Ill appearance – Ill-appearing patients with sinus tachycardia should be assessed for fever and pain. Febrile children warrant careful examination for physical findings of acute rheumatic fever, Kawasaki disease, or sepsis. Severe hypertension, headache, and diaphoresis are seen following the endogenous catecholamine surge that occurs in patients with pheochromocytoma. (See "Acute rheumatic fever: Clinical manifestations and diagnosis" and "Kawasaki disease: Clinical features and diagnosis" and "Pheochromocytoma and paraganglioma in children".)

Well-appearing children with sinus tachycardia usually require no studies if the tachycardia abates with resolution of the suspected underlying cause (eg, a crying child with tachycardia who has a normal rate when quiet). A history of ingestion of caffeinated beverages, diet supplements, herbal preparations, over the counter sympathomimetic or anticholinergic medications, or illicit drugs identifies drug induced sinus tachycardia (table 2).

Patients with pallor should have complete blood and reticulocyte counts drawn to identify and characterize anemia. (See "Approach to the child with anemia".)

Serum thyroid function tests are indicated in children with a goiter or other manifestations of hyperthyroidism. (See "Clinical manifestations and diagnosis of Graves disease in children and adolescents".)

Sinus tachycardia commonly accompanies a visit to the doctor. This situational anxiety and the associated tachycardia typically resolve with reassurance.

Some patients with significant psychiatric distress due to anxiety, panic attack, or other mental illness may also present with palpitations. These patients warrant appropriate workup for potential organic causes, such as hyperthyroidism, and referral to a mental health specialist.

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: Supraventricular arrhythmias".)

SUMMARY AND RECOMMENDATIONS

●Differential diagnosis – The table summarizes the causes of tachycardia, highlighting the most common and the most life threatening causes (table 1). (See 'Differential diagnosis' above.)

●Evaluation – Assessment for shock and the determination of rhythm are two key decision points in the evaluation of children with tachycardia. Children with sinus tachycardia and shock require immediate treatment while the underlying etiology is sought (algorithm 3). (See 'Evaluation' above.)

●Algorithmic approach – The approach to the evaluation and initial management of tachycardia in children are summarized in the algorithms (algorithm 1 and algorithm 2 and algorithm 3 and algorithm 4). (See 'Algorithmic approach' above.)