Pediatric Cardiology Part 2
A Chapter in Core Concepts of Pediatrics, 2nd Edition

Cardiology Part 2: Pediatric EKG Interpretation

shraf Aly MD, PhD

This chapter is designed to cover the essential highlights of pediatric cardiology electrocardiogram (EKG). It is the second part of the Cardiology Chapter in Core Concepts of Pediatrics. It is important that every pediatric provider, not just the cardiologist, understands the basic hemodynamics of the heart and the integration of the cardiovascular system with other body systems.

EKG Interpretation

S. Bhatia, MD, L. Yun, S. Munir, M.E. Gomez, MD A. Aly, MD, PhD

Before you read the EKG, look for:

• Patient age: as many values change with age
• Standardization: full standard is two large squares (1 mV, 10 mm) and half standard is one large square (0.5mV, 5 mm)
• Paper speed: the standard is 25 mm/sec, the faster the paper speed the slower the HR will look and vice versa

Basic EKG interpretation

1. Heart rate: The standard paper speed is 25 mm (5 large squares)/sec. This means that if the interval between two beats (R-R) is 5 large squares, the HR is 60 beat/min.

• The HR may be counted by simply dividing 300 by the number of the large squares between two heart beats (R-R).
• If the interval between two beats is one large square, the HR is 300 beat/min, 2 squares →150, 3 squares →100, 4 squares → 75, 5 squares → 60, 6 squares → 50 beat/min.

2. Rhythm: The cardiac myocytes have an inherent automaticity and can generate an electric impulse. The SA nodal cells have the fastest automaticity (pacemaker) and hence control the heart rate and rhythm. There are 4 levels of conductions and potential pacemakers in the heart from fastest to slowest: SA node → atria → AV node → ventricles. If the rhythm is not sinus, we have to determine the origin of the pacemaker and where the impulse is initiated.

• SA nodal rhythm (normal sinus rhythm) (NSR) (Figure 2)

1. The sinus node is located at the SVC/right atrial junction. Sinus rhythm requires ALL of the following 3 criteria:
1. One P wave preceding each QRS complex
2. All P waves should be uniform in shape
3. Normal P wave axis is in the left lower quadrant (0-90 degrees), i.e. upright in both lead I and aVF (unless there is dextrocardia)
2. The R-R interval in NSR does not have to be identical as it may change with breathing (sinus arrhythmia) (Figure 3.) The sinus arrhythmia is easier to appreciate with slower heart rates.
1. HR increases during inspiration due to:
• Increased venous return
• Increased sympathetic tone
2. HR decreases during expiration due to:
• Decreased venous return
• Increased parasympathetic tone

• Atrial rhythm (Figure 4)

1. Characterized by narrow QRS complexes preceded by P waves that do not fulfill one or more of the normal sinus rhythm (NSR) criteria mentioned earlier.
2. If the P wave morphology changes, this may indicate a multifocal origin which is called "wandering pacemaker".

• AV nodal or junctional rhythm (Figure 5)

1. Characterized by narrow QRS complexes that are not preceded by P waves.
2. An inverted P wave may be seen following the QRS due to retrograde conduction.

• Ventricular rhythm (Fgure 6)

1. Characterized by wide QRS complexes that are not preceded by P waves.

If the sinus node fails to initiate the impulse, an atrial focus will take over as the pacemaker, which is usually slower than the NSR. When the atrial focus fails, the AV node will take over. Subsequently, if the AV node fails, the ventricular focus, which is the slowest, will take over as a pacemaker. Each time the focus is downgraded, the heart rate becomes slower based on the inherent automaticity of the pacemaker.

3. Axis: Determine both P wave and QRS axes. The net summation of positive and negative deflection is used to determine the axis. Look for two perpendicular leads (usually lead I and aVF) to determine in which quadrant the axis is located.

a) If QRS is positive in lead I and positive in aVF, the axis is in the left lower quadrant (0-90 degrees), which is normal
b) If QRS is negative in lead I and positive in aVF, the axis is in the right lower quadrant (90-180 degrees). This represents right axis deviation which can be normal in children.
c) If QRS is positive in lead I and negative in lead aVF, the axis is in the left upper quadrant (-90- 0). This represents left axis deviation.

d. If QRS is negative in lead I and negative in lead aVF, the axis is called indeterminate. Precordial leads may determine if it is an extreme right or left axis deviation.

a) P wave: Represents atrial depolarization. Normally it is 2.5 mm wide and 2.5 mm high.

• Tall P waves = right atrial enlargement (RAE)
• Wide P waves = left atrial enlargement (LAE)
• Wide and tall or bi-peaked P waves = bi-atrial enlargement (BAE).

b) PR interval represents a delay in conduction in the AV node. It varies with age and heart rate and is usually <0.2 sec at any age.

c) QRS duration: Represents ventricular depolarization. Normally 2 small squares or 0.08 sec.

• Wide QRS may indicate:
1. Ventricular contractions
2. Bundle branch block
3. Pre-excitation (Wolff-Parkinson White syndrome)

d) QT interval (measured from the beginning of Q to the end of T wave) represents both ventricular depolarization and repolarization

• QTc is the QT interval corrected for the heart rate. QTc=QT (in seconds)/square root of preceding RR interval (in seconds).
• See causes of long QT syndrome below.

a) Right ventricular hypertrophy (RVH):

1. Voltage criteria (tall R in V1 and deep S in V6>95% for age) (see table below)
2. Right axis deviation
3. rSR' in V1 with a tall R' (> 10 mm)
4. qR pattern in V1;
5. Upright T wave in V1 > 1 week of age
• Newborns have upright T wave in V1
• T wave normally becomes inverted during the first week of life
• Upright T wave beyond the first week of life is a strong indicator of RVH
• T wave remains inverted in V1 throughout early childhood
• T wave becomes upright in V1 in late childhood and early adolescence and is no longer diagnostic of RVH
• ~75% of adults have upright T wave in V1

b) Left ventricular hypertrophy (LVH): Criteria are not as well defined as RVH

1. Voltage criteria (tall R in V6 and deep S in V1);
2. Left axis deviation;
3. Strain pattern in left precordial leads (inverted T waves in V5 and V6)

6. Bundle Branch Block (delay in conduction in either the right or left bundle of His)

Incomplete right bundle branch block (iRBBB, RV conduction delay/ RV volume overload)

1. Narrow QRS complexes
2. RSR' only in V1
3. Does not qualify for RVH criteria

Complete right bundle branch block

1. Wide QRS complexes in all leads preceded by P waves
2. rSR' in V1
3. Terminal slurring (widening of QRS) is positive in V1 and negative in V6

Complete left bundle branch block

1. Wide QRS complexes in all leads preceded by P waves
2. rSR' only in V6
3. Terminal slurring (widening of QRS) is positive in V6 and negative in V1

Arrhythmias

Arrhythmias are defined as disturbances in heart rate and/or conduction. Arrhythmias result from abnormal impulse formation, abnormal impulse conduction, or both. Arrhythmias may occur in children with normal hearts and/or may be associated with CHD, medications or electrolyte disturbances.

Types of Arrrhyhimias

Bradyarrhythmias

Sinus bradycardia

The normal range of heart rate depends on the age of the individual, ranging from 120-160 beat/min in the newborn to 60-80 beat/min in the adult. Trained athletes may normally have sinus bradycardia due to increased vagal tone. Pathological sinus bradycardia is usually secondary to an underlying condition such as hypothyroidism or medications such as beta-blockers.

Asymptomatic physiologic sinus bradycardia requires no treatment. In symptomatic bradycardia, the underlying cause should be treated and a pacemaker placement may be considered if there is no response to medical therapy.

Atrioventricular Block:defect of conduction in the AV node

First degree AV block

This indicates prolongation of the PR interval more than 95th percentile for age and heart rate. At any age, PR interval > 0.2 seconds is considered prolonged.

Causes include:

• Impairment in the AV node conduction caused by increased vagal tone
• AV nodal ischemia
• Drugs such as digoxin and beta-blockers

It is usually reversible and does not require any treatment. First degree AV block could be one of the cardiac manifestations of rheumatic fever.

Second degree AV block

This is secondary to an intermittent failure of conduction through the AV node so that some P waves are not followed by QRS complexes.

Mobitz type I (Wenckebach) is a gradual prolongation of the PR interval until there is a P wave that is not conducted (not followed by a QRS complex). It is usually benign and may be seen in the presence of increased vagal tone, during sleep or in trained athletes.  

Mobitz type II is sudden loss of AV conduction (two or more P waves before QRS complexes). It is more serious as it may progress to a complete AV block. Implantation of a pacemaker may be considered in symptomatic patients.  

Third degree (complete) AV block (atrioventricular dissociation)

Complete AV block represents complete atrioventricular dissociation with no correlation between the atrial and ventricular electrical activity. The ventricular rate is significantly slower than the atrial rate. A pacemaker placement is warranted in symptomatic patients. This condition may be seen in infants born to mothers with systemic lupus erythematosus (SLE).

Tachyarrhythmias

Sinus tachycardia:

Sinus tachycardia is characterized by narrow fast QRS complexes that are preceded by normal P waves. Sinus tachycardia may be a physiologic response to exercise, anxiety, fever, hypovolemia, hypoxemia or hyperthyroidism. A good rule of thumb to remember for fever is 1 degree Celsius increase in temperature accounts for ~10 b/min increase in HR. Maximum physiologic HR is 220 bpm age in years.

Premature atrial complexes (PAC's)

PAC's represent an early atrial electrical activity outside the SA node. PAC's may appear in one of three forms:

1. Premature P wave followed by a narrow QRS complex (conducted PAC)
2. Premature P wave not followed by a QRS complex (non-conducted PAC)
3. Premature P wave followed by wide QRS complex (conducted PAC with aberrancy i.e. bundle branch block)

PAC's are commonly seen in infants and usually disappear with increasing age. It is usually benign and needs no treatment.

Supraventricular Tachycardia (SVT)

SVT is characterized by a narrow QRS complex tachycardia with a heart rate of 250-350 beat/min. It is commonly seen in children with normal hearts but may be associated with some CHD such as Ebstein anomaly. SVT may be caused by an accessory pathway between the atria and the ventricles or by a reentry circuit within the AV node. In infants, SVT presents with poor feeding, irritability, sweating and respiratory distress. Prolonged SVT may lead to CHF due to coronary insufficiency.

Compensated SVT should be treated promptly with vagal maneuvers such as application of ice to the face. If this is unsuccessful, then adenosine should be administered intravenously. Children with uncompensated SVT should undergo cardioversion. Wolff Parkinson White (WPW) syndrome is an example of pre-excitation due to an accessory pathway between the atria and ventricles. It is characterized by short PR intervals, delta waves, and wide QRS complexes.

Ventricular arrhythmias

Ventricular arrhythmias are characterized by wide QRS complexes that are not preceded by P waves, and abnormal T waves. The symptoms depend on the heart rate and are usually due to poor ventricular filling. This is a potentially serious dysrhythmia and synchronized cardioversion is commonly indicated.

Premature ventricular contractions (PVC's)

PVC's are early, wide QRS complexes that are not preceded by P waves. Isolated unifocal PVC's originate from the same spot in the ventricles and have a uniform morphology. They are usually benign in nature and disappear as the heart rate increase with exercise. On the other hand, multifocal PVC's have different morphology as they originate from different foci in the ventricles. They usually occur in diseased myocardium and their frequency often increases with exercise.

Ventricular tachycardia (VT)

VT is a rapid, wide QRS-complex tachycardia with a heart rate 150-250 beat/min. It is a serious condition that may result from drug toxicity (digoxin), myocarditis or severe metabolic derangement. It should be treated promptly with synchronized DC cardioversion if the patient is hemodynamically unstable. Stable VT may be treated with IV lidocaine infusion. Oral amiodarone may be used for outpatient management.

Ventricular Fibrillation (VF)

VF is a serious and terminal cardiac rhythm characterized by irregular, wide bizarre shaped QRS complexes. It needs urgent treatment with unsynchronized DC cardioversion.

 Long QT Syndrome (LQTS)

The QT interval represents both ventricular depolarization and repolarization. The QT interval varies with heart rate. The faster the heart rate, the shorter the QT interval. The corrected QT (QTc) interval is calculated by dividing the measured QT in seconds by the square root of the preceding R-R interval in seconds. A corrected QT greater than 0.46 seconds is considered prolonged. In normal neonates, the QTc may be 0.50 seconds in the first few days of life.

LQTS is an inherited condition characterized by syncope, seizures, palpitations or even sudden death. There are four different classes of patients with LQTS:

1. Jervell and Lange-Nielsen syndrome, which is inherited in an autosomal recessive fashion and is commonly associated with sensorineural deafness
2. Romano-Ward syndrome, which is inherited in an autosomal dominant fashion and is not associated with deafness
3. The QT interval may be prolonged beyond the neonatal period by certain drugs (Table 2), toxins and electrolyte imbalance
4. Sporadic cases of LQTS have also been reported

Table 2: Common drugs which may cause QT prolongation

Pathophysiology

Congenital long QT syndrome may be caused by an imbalance of the sympathetic innervation in the heart especially the stellate ganglion or derangements in the cardiac ion flow, resulting in prolongation of the action potential. During the latter phase of the action potential, the myocardium is very excitable and may develop arrhythmia if stimulated electrically or mechanically. If a PVC occurs during this phase of the action potential (R on T phenomenon), a delayed after-depolarization develops in the form of a specific polymorphic ventricular arrhythmia (Torsades de pointes).

No discernable P waves, wide QRS complexes twisting around isoelectric axis
Dianosis: Torsades de pointes

Clinical

Most patients are asymptomatic. Symptomatic patients present with episodic dizziness, palpitations, syncope, seizures, and/or cardiac arrest. Patients with long QT syndrome can develop Torsades de pointes, bradyarrhythmias, or AV block. This can be triggered by exercise, emotions or loud noises.

Making the Diagnosis

1. Clinical history.
2. Family history of arrhythmia or sudden cardiac death.
3. QTc> 0.46 second (beyond the neonatal period), bradycardia, second degree AVB, multiform PVCs and T wave changes (T wave alternans, bifid T wave or biphasic T wave).
4. Further testing: Holter or event monitors, stress test and other electrophysiologic studies.

Management

LQTS is a serious condition. The risk factors for sudden death include long QT > 0.55 seconds, family history of sudden death, bradycardia for age, and a prior history of symptoms. Any medications that may cause QT prolongation should be discontinued.

Treatment is aimed at preventing conversion to other possibly fatal arrhythmias. Beta-blockers are the mainstays of medical management. An implanted cardioverter-defibrillator (ICD) is often used as a nonpharmacological treatment. Other treatment modalities include permanent dual chamber pacemaker and left cardiac sympathetic denervation.     

EKG Quiz

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References and Resources

2007 Guidelines From the American Heart Association.

Abbreviations for CardiologyChapter

American Academy of Pediatrics

Diagnosis, Treatment, and Long-Term Management of Kawasaki Disease:

Scientific statement from American Heart Association

Resources by Chapter Authors  

Evaluation of the Cyanotic Newborn: Part1 - A Neonatologist's Perspective UTMB password required

Evaluation of the Cyanotic Newborn: Part2 - A Cardiologist's Perspective UTMB password required