Pediatric emergency medicine trisk 381

CHAPTER 77 ■ TACHYCARDIA
STEVEN C. ROGERS, V. MATT LAURICH

INTRODUCTION
Fast heart rate or tachycardia is a common sign in children receiving emergency
care. It may be noticed on initial evaluation by the emergency provider or may be
raised as a concern by the patient or a caregiver who notes a rapid heart rate while
holding the child or observes rapid jugular venous pulsations, increased apical
heart rate, or pulse rate. Normal heart rate varies by age, but there is no
universally accepted definition for tachycardia for any given age. Published
normal ranges by age exist, and even commonly used guidelines and definitions
vary. In infants and young children, the higher resting heart rate, relative to older
children, adolescents, and adults, reflects higher tissue oxygen utilization and
metabolic rate. In most instances, the underlying cause for tachycardia in children
is benign. However, children with a life-threatening etiology for their tachycardia
require prompt recognition and treatment.

PATHOPHYSIOLOGY
Cardiac muscle has intrinsic automaticity that allows it to beat without any
external stimulus. Resting heart rate typically reflects a balance of input from the
vagus nerve (cranial nerve X) and the thoracic sympathetic ganglion (levels T1 to
T4). Vagal stimulation results in slowing of the heart rate mediated by cholinergic
receptors and has a greater impact on resting heart rate than on the sympathetic
nervous system. Thus, medications with anticholinergic receptor effects (e.g.,
antihistamines, atropine) may cause tachycardia. Sympathetic stimulation results
in increased heart rate and force of contraction primarily through the β1 adrenergic receptors. These receptors may also be stimulated by circulating
endogenous substances (e.g., epinephrine, increased carbon dioxide tension,
hypoxemia) and by exogenous agents (e.g., sympathomimetic drugs).
Life-threatening cardiac tachyarrhythmias (e.g., supraventricular tachycardia
[SVT], ventricular tachycardia) arise from various mechanisms that disrupt
normal electrical conduction in the heart. The pathophysiology of these

arrhythmias is discussed separately (see Chapter 86 Cardiac Emergencies ).

DIFFERENTIAL DIAGNOSIS


Many conditions may produce tachycardia ( Table 77.1 ). Most tachycardic
children exhibit sinus tachycardia without significant cardiac pathology ( Table
77.2 ). However, life-threatening conditions frequently come to medical attention
because of fast heart rate and may reflect cardiac and noncardiac origins ( Table
77.3 ).

Sinus Tachycardia
Fever, pain, and emotional arousal (e.g., crying, anxiety) are the most frequent
causes of sinus tachycardia in children. Sympathetic stimulation from other
conditions such as hypoxemia, hypoglycemia, hypercarbia, anemia, and excess
circulating catecholamines (e.g., hyperthyroidism, pheochromocytoma) also
increases sinoatrial node firing rate ( Table 77.2 ). Exogenous sympathomimetic
or anticholinergic substances may cause sinus tachycardia. Over-the-counter
medications that contain antihistamines or pseudoephedrine, “energy” drinks and
diet pills that have high concentrations of caffeine, and commonly abused
substances nicotine (e.g., cigarettes, e-cigarettes/vaping products, gums, patches),
cocaine, amphetamines, methcathinones (e.g., bath salts), or synthetic
cannabinoids (e.g., K2, Spice) are frequently implicated (see Table 63.4 ).
Conversely tachycardia can be a sign of withdrawal from alcohol,
benzodiazepines, or opiates.
Shock is a life-threatening cause of sinus tachycardia that requires rapid
recognition and reversal to prevent permanent organ damage or death (see
Chapter 10 Shock ). Shock may result from intravascular volume loss, inadequate
cardiac contractility, a marked drop in systemic vascular resistance, or a
combination of these mechanisms. History and physical findings help

differentiate the various forms of shock (hypovolemic, cardiogenic, septic, and
distributive) and identify the underlying cause.
Cardiac inflammation associated with viral myocarditis, acute rheumatic fever,
or Kawasaki syndrome frequently presents with sinus tachycardia (see Chapter 86
Cardiac Emergencies ). Patients with these conditions, especially myocarditis, are
also at risk for life-threatening arrhythmias, myocardial ischemia, congestive
heart failure, and/or cardiogenic shock. For patients with pericardial effusion,
sinus tachycardia is a physiologic response to impaired cardiac outflow in order
to maintain cardiac output (see Chapter 86 Cardiac Emergencies ). Pericardial
effusion with tamponade may complicate pericarditis, blunt chest trauma, or
recent cardiac surgery and results in decreased cardiac output with significant
impairment of systemic circulation. In this setting, pericardiocentesis or surgical
pericardiotomy is lifesaving (see Chapter 115 Thoracic Trauma ).


Tachyarrhythmias
SVT represents the most common tachyarrhythmia of childhood (see Chapter 86
Cardiac Emergencies ). The typical heart rate in infants with SVT exceeds 220
beats per minute, whereas older children usually have a heart rate in excess of
180 beats per minute. Infants and children with SVT demonstrate a range of
physical signs including no symptoms, palpitations, chest pain, tachypnea (often
with feeding in infants), diaphoresis, and severe cardiogenic shock.
TABLE 77.1
DIFFERENTIAL DIAGNOSIS OF TACHYCARDIA
Sinus tachycardia
Fever
Crying
Pain
Hypoglycemia
Hypoxemia

Hypercarbia
Shock
Anemia
Poisoning (see Table 63.4 )
Sepsis
Anaphylaxis
Hyperthyroidism
Pheochromocytoma
Drug induced (e.g., antihistamines, caffeine, dietary supplements)
Withdrawal (e.g., alcohol, benzodiazepines, opiates)
Anxiety
Myocarditis
Acute rheumatic fever
Kawasaki disease
Pericardial effusion with tamponade
Tachyarrhythmias
Supraventricular tachycardia
Atrial flutter
Ventricular tachycardia (monomorphic and polymorphic/torsades de pointes)


The most common form of SVT involves an accessory atrioventricular (AV)
pathway. Additional etiologies include drug exposure, congenital heart disease,
and Wolff–Parkinson–White syndrome. Sympathomimetics in cough and cold
preparations are the most common drugs to incite SVT in children. Unregulated
dietary supplements such as ephedra (and its congeners, often advertised as
“ephedra-free” products) and high-caffeine energy drinks also have the potential
to precipitate SVT. Cardiac lesions associated with SVT include Ebstein anomaly,
repaired dextrotransposition of the great arteries, and single-ventricle lesions
status post-Fontan operation.

Ventricular tachycardia (monomorphic or polymorphic/torsades de pointes) and
atrial flutter rarely occur in children (see Chapter 86 Cardiac Emergencies ).
Congenital heart disease, electrolyte disturbance (e.g., hyperkalemia,
hypocalcemia, hypomagnesemia), genetic predisposition (e.g., long QT
syndromes), or poisoning accounts for most cases of ventricular tachycardia in
children. Atrial flutter usually arises from an intra-atrial reentry circuit. Most
children with atrial flutter have congenital heart disease. Although rare, atrial
flutter carries a significant risk of sudden death if not controlled by medications
or surgical intervention.
TABLE 77.2
COMMON CAUSES OF TACHYCARDIA
Fever
Pain
Crying
Anxiety
Anemia
Drug induced (e.g., caffeine, herbal medications, dietary supplements, illicit
drugs)
Hypovolemic shock