Bradycardia is a heart rate below normal range for age with many etiologies. Bradycardia of <60 beats per minute (bpm) associated with poor systemic perfusion is clinically significant. Signs include poor skin perfusion with pallor, cyanosis, cool mottled extremities, prolonged capillary refill, thready, weak, or absent peripheral pulses, and discrepancy in volume between peripheral and central pulses. Patients are irritable, lethargic, confused, or have decreased level of consciousness. Severe bradycardia may cause respiratory difficulty, decreased pulse pressure of >20 mm Hg, hypotension (decompensated shock), and decreased or no urine output. There are several types of bradyarrhythmias including sinus bradycardia, sinus node arrest with a slow junctional or ventricular escape rhythm, and atrioventricular (AV) block.
ECG is necessary to exclude second-degree or complete heart block (CHB), and findings include a slow heart rate with P waves that may or may not be visible. QRS duration is normal or prolonged (depending on the location of the intrinsic cardiac pacemaker). Dissociation of P waves and QRS is seen in CHB. P wave with a normal PR interval preceding each QRS complex is seen in sinus bradycardia.
Figure 5.1 ▪ Sinus Bradycardia.
(A) 12-lead ECG showing a heart rate of 50 bpm. The patient is in sinus rhythm as every QRS is preceded by a P-wave, a QRS complex follows every P-wave, and the P-wave axis is normal. This could be a normal phenomenon in well-trained athletes. (B) An ECG from a different patient also with a slow heart rate. Note the P-wave axis in leads II, III, and aVF. The P-waves are inverted in these leads, suggesting this is not a sinus-rhythm. This patient is in an ectopic atrial rhythm, which is usually normal. (Photo contributor: Shyam Sathanandam, MD.)
Stabilize ABCs and observe and reassess patients with bradycardia not associated with evidence of poor systemic perfusion and admit for continued observation. Consult cardiology for asymptomatic bradycardia from drug ingestion, complete AV block, acquired or congenital heart disease (CHD), or patients with refractory bradycardia that require pacing.
If cardiorespiratory compromise is present, emergent intervention to establish a patent airway and assist breathing with delivery of 100% oxygen. Perform chest compressions if the patient fails to improve (patient remains unresponsive or flaccid with poor systemic perfusion), the heart rate remains <80 bpm in neonates or <60 bpm in infants and children. If there is no response to effective oxygenation and ventilation, give epinephrine. A continuous epinephrine, isuprel, or dopamine infusion titrated to effect may be required. For symptomatic bradycardia due to vagal stimulation, cholinergic drug toxicity, or primary AV block, give atropine as the drug of choice. Atropine usually is not effective for hypoxic-ischemic induced bradycardia. Vagally induced bradycardia usually resolves once the stimulation is withdrawn. Atropine is very effective if used prophylactically before vagal stimulation in procedures such as endotracheal intubation.
Figure 5.2 ▪ Differential Diagnosis of Bradycardia. Subarachnoid Hemorrhage (SAH) Presenting with Cushing Triad.
A noncontrast head CT scan shows hyperdensity in the basal cisterns in the area of circle of Willis, with blood in the fourth ventricle (findings typical of SAH) in an adolescent boy presenting to the emergency department with sudden onset of severe headache, increasing lethargy, and obtundation. Patient had bradycardia, irregular respirations, and hypertension (Cushing triad secondary to increased intracranial pressure). (Photo contributor: Mark Silverberg, MD.)
Pacing is not helpful in children with bradycardia secondary to postarrest hypoxic-ischemic myocardial insult. It may be helpful for bradycardia caused by acquired or CHD causing CHB or sinus node dysfunction. Options include transcutaneous, transvenous, or transesophageal pacing.
Asymptomatic sinus bradycardia can occur as a normal variant during deep sleep and is also common in highly trained athletes.
Most common causes of symptomatic bradycardia are hypoxemia and vagal stimulation, and if not corrected may degenerate into full cardiac arrest.
| Age | Awake heart rate in bpm (mean) |
| Newborn | 80–180 (130) |
| 1 week to 3 months | 80–180 (140) |
| 3 months to 2 years | 80–160 (130) |
| 2 to 10 years | 65–130 (80) |
| 10 years to adult | 55–90 (75) |
| Etiologies of Bradycardia | |
Respiratory
| |
| Hypoxemia | Tension pneumothorax |
| Hypovolemia | Tamponade |
| Heart block | Toxins/poisons/drugs (eg, organophosphates, clonidine, beta-blockers, calcium channel blockers) |
| Hypothermia | |
| Head injury | |
| Hyperkalemia | |
First-degree AV block is prolongation of the PR interval beyond the norm for age. PR interval is determined by the point of conduction from the sinus node to the onset of QRS. The PR interval and QRS duration are age-dependent measures of AV conduction. Impaired conduction is classified as first-degree, second-degree, or third-degree heart block. The normal PR interval changes with both age and heart rate, but it is more age dependent. The AV node is usually the site of conduction delay, although it may occur in the atrium or the infranodal level. ECG findings of first-degree AV block includes a regular rhythm that originates in the sinus node with a prolonged PR interval and a normal QRS morphology, and etiologies are mentioned in Table 5.3.
Consult cardiology and hospitalize patients with first-degree heart block associated with underlying serious heart disease (eg, acute rheumatic fever, myocarditis) for evaluation and appropriate therapy.
Figure 5.3 ▪ First-Degree Heart Block.
A 12-lead ECG demonstrates a heart rate of 94 bpm and the rhythm is sinus. The PR interval measures 160 ms, demonstrating first-degree AV block in a patient presenting with acute rheumatic fever (ARF). Prolongation of the PR interval is among the minor modified Jones criteria required for the diagnosis of ARF. The PR interval is measured from the beginning of the P-wave to the beginning of the QRS complex. (Photo contributor: Shyam Sathanandam, MD.)
Figure 5.4 ▪ Hyperkalemia Presenting with First-Degree Heart Block.
A 12-lead ECG obtained on a 15-year old boy who presented to the emergency department with respiratory distress and syncope. The ECG shows sinus rhythm, 92 bpm, first-degree AV block (PR = 0.21 sec), broad notched P-waves, left bundle branch block, diffuse ST abnormalities, and tall tented T-waves. His serum potassium level was 7.6 secondary to renal failure. (Photo contributor: Shyam Sathanandam, MD.)
First-degree AV block alone does not lead to hemodynamic compromise and does not need any specific therapy.
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| Conditions Associated with First—Degree AV Block |
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Second-degree AV block is when one or more (but not all) of the atrial impulses fail to conduct to the ventricles because of impaired conduction. Two distinct types of second-degree AV blocks are type I, second-degree AV block (also known as Mobitz I or Wenckebach periodicity) and type II second-degree AV block (also known as Mobitz II). Mobitz type I heart block can occur as a normal variant (without any symptoms) in children. Causes of second-degree AV block include myocarditis, atrial septal defect, acute rheumatic fever, Ebstein anomaly, cardiomyopathy, structural congenital heart disease, drug toxicity (eg, digitalis, beta-blockers), increased vagal tone (any etiology), and following surgery near the AV junction. Patients with Mobitz type II may present with syncope or heart failure. Diagnosis is confirmed by ECG. A chest radiograph may show cardiomegaly, depending on the underlying etiology (eg, myocarditis, cardiomyopathy).
Evaluate patient and consult cardiology to determine the underlying etiology for the second-degree heart block. Admit newly diagnosed patients, those with postcardiac surgery heart block, and symptomatic patients (eg, syncope or dizzy spells) as they may need pacemaker implantation. Treat the underlying cause in patients with Mobitz type I AV block. The prognosis of Mobitz type II AV block associated with a wide QRS complex may progress to complete heart block (CHB). If signs of hypoperfusion are present with slow ventricular rates, give atropine emergently. Alternatively, Isoproterenol can be used with caution (eg, in patients with digoxin toxicity). Transcutaneous cardiac pacing may be required for patients who do not respond to atropine. A permanent transvenous cardiac pacemaker is required if symptoms of presyncope or syncope occur.
Figure 5.5 ▪ Mobitz Type I Second-Degree Heart Block or Wenckebach Periodicity.
A 12-lead ECG demonstrates a progressive prolongation of the PR interval seen on the ECG on consecutive beats followed by a blocked P-wave. This is because of the decremental property of the AV node. After the dropped QRS complex, the PR interval resets and the cycle repeats giving the impression of paired QRS complexes. (Photo contributor: Shyam Sathanandam, MD.)
Figure 5.6 ▪ Mobitz Type II Second-Degree Heart Block.
A rhythm strip demonstrating 3:1 AV block. The atrial rate as measured by the P-P interval is 100/min, but only every third P-wave is followed by a QRS complex. The PR interval is normal, suggesting the level of block is not at the level of the AV node or above the AV node. This type of second-degree AV block called Mobitz type II block is more pathologic as the site of the block is in the more distal conduction system (His-Purkinje system). (Photo contributor: Shyam Sathanandam, MD.)
Mobitz type I heart block is often transient (eg, seen with myocarditis).
Mobitz type II heart block is usually permanent, and implies structural damage to the infranodal conducting system.
| Mobitz Type I AV Block (Wenckebach Block) |
Characteristic features:
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| Mobitz Type II AV Block |
Characteristic features:
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Third-degree AV block, or CHB, occurs when no impulses from the atria reach the ventricles. Because the impulse is blocked, an accessory pacemaker will typically activate the ventricles (an escape rhythm). Third-degree heart block is rare in the pediatric age group. Signs and symptoms in patients with an otherwise normal heart vary. Patients may be bradycardic and asymptomatic. Older children may present with syncope (syncope from a high-degree AV block not related to positional changes or exertion is called a Stokes-Adams attack). Older infants may present with night terrors, irritability, or tiredness with frequent naps. Acquired heart block is frequently symptomatic, or present with syncope, congestive heart failure (CHF), shock, or sudden death. Peripheral pulses may be prominent secondary to large compensatory stroke volume. Chest radiograph may show cardiomegaly secondary to increased diastolic ventricular filling.
Admit symptomatic patients (eg, syncope, CHF) or those newly diagnosed with CHB. Symptomatic newborns (eg, heart failure, evidence of hydrops) with CHB with ventricular rates ≤50 bpm require cardiac pacing. Adrenergic agents (epinephrine or isoproterenol) or a vagolytic agent (atropine) may be tried to increase the heart rate while awaiting placement of the pacemaker. Cardiac pacing (transthoracic, transcutaneous, or transvenous) is also required in symptomatic patients with CHB and CHD. Temporary pacing may be required in postoperative CHB following surgery for CHD.
Figure 5.7 ▪ Complete Heart Block.
A 12-lead ECG demonstrates a third-degree AV block with an atrial rate of 92/min and the ventricular rate of 42/min. There is no constant relationship between the P-waves and the QRS complexes demonstrating atrioventricular dissociation. (Photo contributor: Shyam Sathanandam, MD.)
Autoimmune disease accounts for 60% to 70% of all cases of congenital CHB.
About 25% to 33% of cases of CHB occur in patients with associated structural heart disease.
Complete heart block may not present at birth in infants born to mothers with systemic lupus erythematosus (SLE), and may develop within the first 3 to 6 months after birth. Unlike other manifestations of neonatal lupus that resolve, CHB is permanent and patients often require cardiac pacing.
An implantable pacemaker is used to prevent sudden death in symptomatic patents with CHB.
Characteristic features:
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Some examples of congenital or acquired diseases leading to complete heart block
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Long QT syndrome (LQTS) is a pathologically prolonged corrected QT interval that may be acquired, but more often is congenital and inherited. Prolongation of the QTc interval results from a prolongation of the refractory period of the myocardium (during which the atrium is still firing at its regular pace), leading to torsades de pointes (“R-on-T phenomenon,” a malignant form of ventricular tachycardia [VT]). Patients present with syncope or presyncope episodes (recurrent, often precipitated by exercise, fright, or being startled), seizures or episodes of paroxysmal VT (often with torsades de pointes morphology that can progress to ventricular fibrillation and sudden death). LQTS may be an incidental ECG finding. There may be a family history of sudden death in young relatives, syncope with exercise or emotional stress, seizures, arrhythmias, and hearing impairment (congenital LQTS). The QT interval may be so prolonged in neonates that it may lead to second-degree or complete heart block.
Treatment of VT associated with LQTS includes support of airway, breathing, and circulation (ABCs) and providing oxygen and ventilation as needed. Intravenous lidocaine, or amiodarone, or procainamide can be used. If the above medical therapy fails, synchronized cardioversion is used for stable patients with VT with palpable pulses and defibrillation for patients with pulseless VT as per PALS protocols.
Consult cardiology for any patient with LQTS. ECG features of LQTS include low heart rate for age, notched T waves, and T-wave alternans. Stress testing (exertional LQTS), or 24-hour Holter monitoring (intermittent LQTS) may help in arriving at the final diagnosis. Long-term goals of therapy of LQTS include beta-blockade (propranolol is drug of choice) to prevent VT from progressing to ventricular fibrillation and sudden death and to blunt heart rate response to exercise. Therapy should be continued for life. A pacemaker may be required in some patients to overcome profound bradycardia (a common association). Exercise restriction, and avoiding drugs that are known to cause prolongation of the QT interval (see Syncope) are recommended. Advise parents to learn cardiopulmonary resuscitation (as exercise restriction and drug therapy may be ineffective for some children). An implantable cardioverter-defibrillator may be considered in patients with continued episodes of syncope in spite of therapy, and in those with a history of cardiac arrest.
Figure 5.8 ▪ Prolonged QT Interval.
A 12-lead ECG demonstrates sinus rhythm with a rate of 95 bpm. There is 1:1 AV conduction. The PR interval and QRS duration are normal. The QT interval is prolonged and the QTc measures 580 ms. This patient presented with syncope during exercise and was found to have long QT syndrome. (Photo contributor: Shyam Sathanandam, MD.)
Figure 5.9 ▪ Long QT Syndrome (LQTS) with 2:1 Block.
A 12-lead ECG obtained from a neonate with LQTS. The QTc is 600 ms. There is 2:1 AV block with an atrial rate of 140 and ventricular rate of 70 bpm. LQTS associated with heart block leads to a worse prognosis and pacemaker insertion is indicated. (Photo contributor: Shyam Sathanandam, MD.)
Patients with LQTS may have a normal ECG in the emergency department (ED).
Congenital LQTS results in a mortality rate in excess of 90% if not diagnosed and properly treated.
LQTS in association with hypertrophic cardiomyopathy accounts for up to half of the cases of sudden cardiac death.
Children with LQTS are predisposed to episodic ventricular arrhythmias, torsades de pointes, syncope, and generalized seizures.
Patients with LQTS may develop fatal ventricular arrhythmias, especially if exposed to some medications such as antihistamines, macrolide antibiotics, or phenothiazines.
All family members of a patient with LQTS should undergo a 12-lead ECG (and cardiac evaluation as indicated).
Any patient presenting with VT (especially torsades de pointes or a polymorphic type) should have a corrected QT interval determined while in sinus rhythm.
Figure 5.10 ▪ Long QT Syndrome: Polymor-Phic Ventricular Tachycardia (VT).
A 6-lead ECG obtained on a 12-year-old girl who presented to the emergency department with palpitation on and off and syncope. The ECG demonstrates that the child has long QT interval, which lead to polymorphic VT while the ECG was being recorded. She went in and out of VT leading to symptoms. An intravenous infusion of magnesium sulfate or a b-blocker could stop this from progressing to full blown VT. (Photo contributor: Shyam Sathanandam, MD.)
Figure 5.11 ▪ Long QT Syndrome (LQTS) with Complete Heart Block.
A 12-lead ECG showing LQTS in a neonate. The QTc is 600 ms. There is a complete heart block with an atrial rate of 144 and ventricular rate of 40 bpm. There is no constant relationship between the P-waves and the QRS complexes. LQTS associated with heart block leads to a worse prognosis and pacemaker insertion is indicated. (Photo contributor: Shyam Sathanandam, MD.)
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| Etiology of Prolonged QT Interval |
Congenital (about 50% of cases):
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Acquired:
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Syncope is a sudden and brief loss of consciousness accompanied by a loss of postural tone with spontaneous recovery. It result from a sudden decrease or brief cessation of cerebral blood flow.
Vasovagal syncope (neurocardiogenic syncope, fainting spell) is the most common and includes emotional fainting, situational syncope, syncope with panic, and syncope associated with exercise in athletes (without heart disease). Vasovagal syncope is usually seen in adolescents and most often occurs after prolonged standing (eg, crowded, warm environment), or with noxious stimuli, strong emotions, or fatigue.
Orthostatic syncope occurs while standing or during a rapid change from supine or sitting position to standing. Measure orthostatic blood pressure (BP) 3 minutes after patient stands up following a supine period of 5 minutes (orthostatic changes present if BP changes >15 mm Hg and HR changes >10 bpm). Predisposing events include dehydration, acute blood loss, or vasodilator drugs.
Cardiac syncope results from hypoxemia due to cyanotic heart disease or decreased cardiac output secondary to arrhythmia, obstructive lesion, or myocardial dysfunction. Syncope occurs during physical exertion (eg, LQTS). Syncope occurs suddenly without warning.
Breath-holding spells are commonly seen between 1 and 5 years of age (peaks around 2 years of age) and resolves spontaneously by school age. There are two major types: cyanotic type (about 80%) and pallid type (about 20%). Provoking events include pain, anger, frustration, vigorous crying followed by forced expiration and apnea (breath-holding spell). Unconsciousness occurs due to decreased cardiac output. Generalized clonic jerks, opisthotonus, and bradycardia and incontinence may occur. Normal physical examination (including cardiac and neurologic) is a hallmark.
Figure 5.12 ▪ Paced Rhythm.
A 12-lead ECG demonstrates electronic pacemaker activity. The patent is being paced VVI at a rate of 100. Any patient with a pacemaker presenting with syncope should get a 12-lead ECG and interrogation of the pacemaker to rule out pacemaker malfunction. (Photo contributor: Shyam Sathanandam, MD.)
Figure 5.13 ▪ Cardiac Tumor Presenting with Recurrent Syncope.
(A) Squatting position assumed by patient while “feeling tired”. This previously healthy 10-year old presented with recurrent syncope and weakness, increasing tiredness, and shortness of breath of 2 weeks -duration. He had hypotension with blood pressure of 87/63 mm Hg (Remember: The median systolic BP for children older than 1 year is 90 + [2 × age in years], and the lower limit is 70 + [2 × age in years]), heart rate of 90 bpm and a normal cardiac examination. Hepatomegaly, right atrial enlargement on ECG and mild cardiomegaly on chest radiograph were also noted. (B) Right atrial mass (arrow) obstructing right ventricular inflow tract on echocardiography. This 6.5 × 5.5 × 4 cm mass was resected and was found to be precursor B lymphoblastic lymphoma/leukemia (intracardiac lymphoblastic lymphoma). (Photo contributors: Barry Hahn, MD and Sudha Rao, MD.)
Determine the degree of hemodynamic stability including orthostatic BP and HR measurements. Specific treatment of syncope depends on the underlying etiology (eg, LQTS). Routine basic laboratory tests (eg, CBC, electrolytes, glucose) are rarely helpful. Obtain additional tests as guided by the history and examination (eg, toxicology screen, carboxyhemoglobin). Exclude pregnancy in adolescent girls. Obtain a 12-lead ECG (with rhythm strip) in all patients (in spite of its low yield) because findings can lead to specific therapy (eg, pacemaker for complete heart block, beta-blocker for LQTS). Arrhythmias that lead to syncope may not be present. Consider 24-hour Holter monitoring. Consult cardiology if cardiac syncope is likely based on history/examination or abnormal ECG findings or syncope with chest pain, arrhythmias, or palpitations, or a family history of sudden death. Consult neurology if seizures cannot be excluded based on the history or with an abnormal neurologic examination.
Reassure and educate patients about the benign nature of vasovagal syncope, identifying and avoiding precipitating factors (eg, dehydration, ensure intake of salty foods during intense physical activity). Advise patients to learn to recognize prodromal symptoms and assume a sitting or supine position with elevation of the feet. For orthostatic syncope, provide fluid therapy to patients with volume depletion. Encourage patients to get up slowly after lying or sitting and discontinue or reduce the dose of any medication that may be responsible.
Figure 5.14 ▪ Cardiac Tumor Presenting with Recurrent Syncope.
(A) Four-chamber view of a 3D echo in a young patient with recurrent syncope. There is a large tumor (arrow) in the interventricular septum that probably caused syncope secondary to obstruction of the left ventricular outflow tract. (B) A parasternal short axis view shows the large tumor in the interventricular septum (arrow). Primary intracardiac tumor in infants is most likely benign rhabdomyoma that usually regresses and <50% of these patients have tuberous sclerosis. (Photo contributor: Shyam Sathanandam, MD.)
Admit patients presenting with recurrent syncope of undetermined etiology, cardiac syncope (eg, LQTS tachyarrhythmia, or symptoms suggestive of arrhythmias [eg, syncope associated with palpitations, exertional syncope], atrioventricular block, valvular or congenital heart disease, pacemaker malfunction, congestive heart failure, cyanotic spells).
Syncope is a symptom, not a disease.
A thorough history and physical examination are essential for the evaluation of syncope and may lead to or suggest a diagnosis that can be evaluated with directed testing.
Vasovagal syncope is the most common cause of fainting in children and adolescents and accounts for >50% of cases of childhood syncope.
Dizziness, vertigo, and presyncope do not result in loss of consciousness or postural tone.
Cardiac syncope (cardiac lesions producing syncope):
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Noncardiac syncope:
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| Syncope | Seizures | |
|---|---|---|
| Precipitants of episodes: | ||
| Pain, exercise, stressful event, micturition, defecation | Usually present | Absent |
| Symptoms before or during episode | Sweating, nausea, feeling of “passing out” | Aura may be present |
| Disorientation after event | Absent | Present |
| Slowness in regaining consciousness | Absent | Present |
| Confusion on awakening | Absent or mild | Marked |
| Period of unconsciousness | Usually seconds | Minutes or longer |
| Unconsciousness >5 minutes | Absent | May be present |
| Rhythmic movements: | ||
| Tonic-clonic movements, myoclonic jerks | Occasionally seen | Commonly seen |
| Incontinence during episode | Absent | May be present |
| Electroencephalogram | Normal | May be abnormal |
Sinus tachycardia (ST) is a rate of sinus node discharge higher than normal for the patient’s age (see Table 5.1). The usual upper limit in infants and young children (up to 5 years old) is up to 200 bpm. The upper limit in older children is up to 180 bpm. Tachycardia is a physiological response to the body’s need for increased cardiac output (CO) or oxygen delivery (tachycardia is the first sign of hypovolemia: CO = SV × HR; thus to maintain cardiac output, a compensatory increase in HR occurs, as the child’s ability to increase stroke volume [SV] is limited). ST is a nonspecific sign of an underlying condition rather than a true arrhythmia. On an ECG, all P waves are normal in configuration (upright in lead II), all QRS complexes are preceded by a P wave. The P-, QRS-, and T-wave morphology are normal.
Use continuous cardiac and pulse oximetry monitoring for patients presenting with ST near the range of supraventricular tachycardia (SVT) (eg, HR approaching 200 bpm), and treat the underlying cause of ST: antipyretics for fever, oxygen therapy for hypoxia, fluid therapy for hypovolemia, pain management. Do not attempt to decrease heart rate with pharmacologic or electrical intervention. ST usually resolves once the stressor ceases and the heart rate returns to normal levels with appropriate treatment of the underlying cause.
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