This document discusses common pediatric arrhythmias seen on electrocardiograms (ECGs). It describes bradyarrhythmias like sinus bradycardia and sinus arrest. It also discusses atrioventricular blocks including first-degree, second-degree (Wenckbach and Mobitz), and third-degree heart block. It describes normal QRS duration tachycardias like sinus tachycardia and supraventricular tachycardias. The document provides ECG examples and classifications of various arrhythmias seen in pediatric patients.
A 30-year-old man presented to the emergency department with palpitations and tachycardia.He had been experiencing sore throat, fevers, andmyalgias for the past day.He became
alarmed when he awoke from sleep with strong palpitations and a heart rate greater
than 200/min documented on his smartwatch.Hehad similar symptoms1 year ago andwas diagnosed with and treated for supraventricular tachycardia (SVT). A subsequent outpatient
echocardiogram revealed a structurally normal heart; results of a follow-up electrocardiogram (ECG) were also normal
Left ventricular false tendons (LVFTs) are fibromuscular
structures, connecting the left ventricular
free wall or papillary muscle and the ventricular
septum.
There is some discussion about safety issues during
intense exercise in athletes with LVFTs, as these
bands have been associated with ventricular arrhythmias
and abnormal cardiac remodelling. However,
presence of LVFTs appears to be much more common
than previously noted as imaging techniques
have improved and the association between LVFTs
and abnormal remodelling could very well be explained
by better visibility in a dilated left ventricular
lumen.
Although LVFTsmay result in electrocardiographic abnormalities
and could form a substrate for ventricular
arrhythmias, it should be considered as a normal
anatomic variant. Persons with LVFTs do not appear
to have increased risk for ventricular arrhythmias or
sudden cardiac death.
Some slides are taken from different textbooks of medicine like Davidson, Kumar and Clark and Oxford, and some from other presentations made by respected tutors. I'm barely responsible for compilation of various resources per my interest. These resources are free for use, and I do not claim any copyright. Hoping knowledge remains free for all, forever.
A 30-year-old man presented to the emergency department with palpitations and tachycardia.He had been experiencing sore throat, fevers, andmyalgias for the past day.He became
alarmed when he awoke from sleep with strong palpitations and a heart rate greater
than 200/min documented on his smartwatch.Hehad similar symptoms1 year ago andwas diagnosed with and treated for supraventricular tachycardia (SVT). A subsequent outpatient
echocardiogram revealed a structurally normal heart; results of a follow-up electrocardiogram (ECG) were also normal
Left ventricular false tendons (LVFTs) are fibromuscular
structures, connecting the left ventricular
free wall or papillary muscle and the ventricular
septum.
There is some discussion about safety issues during
intense exercise in athletes with LVFTs, as these
bands have been associated with ventricular arrhythmias
and abnormal cardiac remodelling. However,
presence of LVFTs appears to be much more common
than previously noted as imaging techniques
have improved and the association between LVFTs
and abnormal remodelling could very well be explained
by better visibility in a dilated left ventricular
lumen.
Although LVFTsmay result in electrocardiographic abnormalities
and could form a substrate for ventricular
arrhythmias, it should be considered as a normal
anatomic variant. Persons with LVFTs do not appear
to have increased risk for ventricular arrhythmias or
sudden cardiac death.
Some slides are taken from different textbooks of medicine like Davidson, Kumar and Clark and Oxford, and some from other presentations made by respected tutors. I'm barely responsible for compilation of various resources per my interest. These resources are free for use, and I do not claim any copyright. Hoping knowledge remains free for all, forever.
12-lead electrocardiogram features of arrhythmic risk: A focus on early repolarization
Caterina Rizzo, Francesco Monitillo, Massimo Iacoviello
Caterina Rizzo, Francesco Monitillo, School of Cardiology, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, Italy
Massimo Iacoviello, Cardiology Unit, Department of Cardiothoracic, Policlinic University Hospital, 70124 Bari, Italy
His Resynchronization VersusBiventricular Pacing inPatients With Heart Fail...Shadab Ahmad
This study tested the ability of HBP to deliver resynchronization and then compared the electromechanical effects of His resynchronization against conventional BVP, using high-precision hemodynamic assessment and noninvasive epicardial ventricular activation mapping
In this ppt i am going to discuss various spotters, including ECG, X-ray, fluroscopy images and there answers. These spotter now days asked in various DM cardiology exam conducted all over India, so it will help you in your DM Cardiology exam preperationn.
Brugada syndrome (BrS) is an inherited cardiac disorder,
characterised by a typical ECG pattern and an increased
risk of arrhythmias and sudden cardiac death (SCD).
BrS is a challenging entity, in regard to diagnosis as
well as arrhythmia risk prediction and management.
Nowadays, asymptomatic patients represent the majority
of newly diagnosed patients with BrS, and its incidence
is expected to rise due to (genetic) family screening.
Progress in our understanding of the genetic and
molecular pathophysiology is limited by the absence
of a true gold standard, with consensus on its clinical
definition changing over time. Nevertheless, novel
insights continue to arise from detailed and in-depth
studies, including the complex genetic and molecular
basis. This includes the increasingly recognised
relevance of an underlying structural substrate. Risk
stratification in patients with BrS remains challenging,
particularly in those who are asymptomatic, but recent
studies have demonstrated the potential usefulness
of risk scores to identify patients at high risk of
arrhythmia and SCD. Development and validation of
a model that incorporates clinical and genetic factors,
comorbidities, age and gender, and environmental
aspects may facilitate improved prediction of disease
expressivity and arrhythmia/SCD risk, and potentially
guide patient management and therapy. This review
provides an update of the diagnosis, pathophysiology
and management of BrS, and discusses its future
perspectives.
12-lead electrocardiogram features of arrhythmic risk: A focus on early repolarization
Caterina Rizzo, Francesco Monitillo, Massimo Iacoviello
Caterina Rizzo, Francesco Monitillo, School of Cardiology, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, Italy
Massimo Iacoviello, Cardiology Unit, Department of Cardiothoracic, Policlinic University Hospital, 70124 Bari, Italy
His Resynchronization VersusBiventricular Pacing inPatients With Heart Fail...Shadab Ahmad
This study tested the ability of HBP to deliver resynchronization and then compared the electromechanical effects of His resynchronization against conventional BVP, using high-precision hemodynamic assessment and noninvasive epicardial ventricular activation mapping
In this ppt i am going to discuss various spotters, including ECG, X-ray, fluroscopy images and there answers. These spotter now days asked in various DM cardiology exam conducted all over India, so it will help you in your DM Cardiology exam preperationn.
Brugada syndrome (BrS) is an inherited cardiac disorder,
characterised by a typical ECG pattern and an increased
risk of arrhythmias and sudden cardiac death (SCD).
BrS is a challenging entity, in regard to diagnosis as
well as arrhythmia risk prediction and management.
Nowadays, asymptomatic patients represent the majority
of newly diagnosed patients with BrS, and its incidence
is expected to rise due to (genetic) family screening.
Progress in our understanding of the genetic and
molecular pathophysiology is limited by the absence
of a true gold standard, with consensus on its clinical
definition changing over time. Nevertheless, novel
insights continue to arise from detailed and in-depth
studies, including the complex genetic and molecular
basis. This includes the increasingly recognised
relevance of an underlying structural substrate. Risk
stratification in patients with BrS remains challenging,
particularly in those who are asymptomatic, but recent
studies have demonstrated the potential usefulness
of risk scores to identify patients at high risk of
arrhythmia and SCD. Development and validation of
a model that incorporates clinical and genetic factors,
comorbidities, age and gender, and environmental
aspects may facilitate improved prediction of disease
expressivity and arrhythmia/SCD risk, and potentially
guide patient management and therapy. This review
provides an update of the diagnosis, pathophysiology
and management of BrS, and discusses its future
perspectives.
An ECG Monitoring Paediatric might be referred to as a piece of the evaluation of a tremendous number of issues in pediatrics, routinely in patients who have no clinical proof of coronary illness. Generally speaking, the deals is made by specialists with no specific wellness in cardiology
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
2. diagnosis, particularly with regard to sleeping vs the waking
state and level of athletic training.
Sinus arrest (also known as sinus pause) reflects the
failure of the sinoatrial node to propagate impulses. If the
period of arrest is prolonged, escape rhythms may “take
over” the function of the sinoatrial, and these escape rhythms
may occur at the AV nodal, bundle of His, or ventricular
level. In children, the mean maximum duration of sinus
pause (F2 SD) was found to be 1.82 seconds [2].
3. Atrioventricular block
The generic term AV block implies a disturbance of
impulse conduction from the atria to the ventricles. The
anatomic locations of such disturbances vary depending on
the underlying mechanism of the arrhythmia. Generally, AV
block is categorized into first-degree (1°), second-degree
(2°), and third-degree (3°) subtypes. First-degree block
(Fig. 2) is identified electrocardiographically by a prolonged
Fig. 1 Sinus bradycardia in a child with hypothyroidism. The heart rate varies between 30 and 40 bpm.
Fig. 2 First-degree AV block in a young boy undergoing Holter monitoring. Note the markedly prolonged PR interval.
349The pediatric ECG
3. PR interval for age. The reader is referred to age-related
pediatric norms as discussed in Part I and other age-related
norms discussed in this article [3]. First-degree block is
typically asymptomatic and generally does not imply
underlying disease of the conduction system. It may be
seen in the sleeping state [4], in trained athletes with low
resting heart rates [5], and rarely in Lyme disease and
myocarditis [6].
Second-degree AV block is divided into 2 categories: type
I (Wenkebach), in which there is progressive prolongation of
the PR interval until failure of AV conduction occurs
(Fig. 3A), and type II (Möbitz), in which random “dropping”
or failure of AV conduction occurs without PR prolongation
(Fig. 3B). Of the two, type II block is more ominous and may
progress to complete (3°) heart block. Type I 2° block is
again a common variant of normal, particularly in trained
athletes [5]. It is also common after repair of structural
congenital heart disease [7]. The presence of Möbitz block or
any symptomatic 2° block warrants pediatric cardiology
consultation with consideration given to pacing.
Complete or 3° heart block is defined by the absence of
conduction between the atria and ventricles. Complete heart
Fig. 3 A, Type I second-degree AV block from a Holter recording in a 7-year-old boy with congenital complete heart block. B, Type II
second-degree AV block with wide QRS complex.
Fig. 4 Third-degree AV block seen in the same patient as in Fig. 3A. Note that there is no relationship between P waves and QRS complexes.
350 M. O’Connor et al.
4. block is manifested by AV dissociation in which regularly
spaced P waves are not related temporally to the ventricular
escape rhythm (Fig. 4). The QRS duration may be normal or
prolonged depending on the location of the block; more
proximal blocks (ie, near the AV node) will typically result in
a normal QRS duration. Congenital complete heart block
occurs in infants of mothers carrying anti-Ro and anti-La
antibodies; mothers may or may not have clinical symptoms
of lupus [8]. Complete heart block is also a known
complication of surgery for congenital heart disease and
has a significant effect on morbidity and mortality [9].
Complete heart block is almost always symptomatic and
usually requires dual-chamber pacemaker implantation.
The bundle branches are the downstream limbs of the
bundle of His and allow for nearly synchronous depolariza-
tion of the left and right ventricles, which is important in
maintaining cardiac synchrony. Prolongation of conduction
through the bundle branches results in QRS prolongation and
is known as bundle branch block (BBB). Bundle branch
block can affect the right or left bundle branches (RBBB,
LBBB) and be classified as complete or incomplete, based
upon whether there is QRS prolongation for age. Incomplete
RBBB is commonly seen in pediatric ECGs and is
manifested by an rSR′ pattern in lead V1 and a small S
wave in lead V6; the initial upstroke of the QRS is normal
with a delay in the terminal portion of the QRS complex
(Fig. 5). Right bundle branch block is detected in V1; the
Fig. 5 Incomplete RBBB in a 3-week-old male infant after
tetralogy of Fallot repair. Note the rSR′ pattern in leads V1 and V2
with minimal QRS prolongation.
Fig. 6 Complete RBBB in a 19-year-old adolescent girl with
repaired tetralogy of Fallot. Note the similarity of the rSR′ pattern to
the previous figure, with this ECG manifesting QRS prolongation.
Fig. 7 Left bundle branch block. Note the prolonged QRS
duration in the lateral precordial lead V5.
351The pediatric ECG
5. initial upstroke of the QRS is delayed (Fig. 6) with the
terminal portion of normal duration, whereas LBBB is
typically manifested by QRS prolongation in V6 (Fig. 7).
Bundle branch blocks may be seen in a variety of conditions
and is a frequent finding after surgery for congenital heart
disease, particularly in which there has been a ventriculot-
omy (ie, tetralogy of Fallot) [10].
4. Normal QRS duration tachycardias
Numerous schemes exist for classifying tachycardias; a
useful and simple way is to categorize them based upon the
QRS duration. In general, tachycardias with a normal QRS
duration for age can be considered as originating superior to
the AV node, whereas tachycardias associated with QRS
prolongation typically originate at locations inferior to the
AV node. This scheme is not perfect but allows for ease
of organization.
Sinus tachycardia is usually simple to recognize on the
ECG (Fig. 8). For the diagnosis of sinus tachycardia to be
established, a P wave must precede every QRS complex and
the P waves must have a normal axis (discussed previously).
In adults, a heart rate greater than 100 bpm is considered
tachycardia. In children, this rate is age dependent but
general guidelines exist; heart rates greater than 160 bpm in
infants and greater than 140 bpm in children suggest sinus
tachycardia [11]. Sinus tachycardia often reflects anxiety,
dehydration, or fever, and can be considered an “appropriate”
physiologic response to the underlying disturbance. “Inap-
propriate” sinus tachycardia implies underlying primary
cardiac disturbance and is often seen in myocarditis or
congestive heart failure. Although a wide range of heart rates
may be seen in sinus tachycardia, the sinus node rarely paces
at heart rates greater than 220 bpm; when greater heart rates
are seen, sinus tachycardia is uncommon. Ectopic atrial
tachycardias can be difficult to distinguish from so-called
supraventricular tachycardias (SVTs; see below), particu-
larly at high rates in which the P wave is “buried” within the
T wave of the preceding QRS complex (Fig. 9).
Atrial flutter and atrial fibrillation are quite rare in
pediatric patients. However, a form of atrial flutter can be
seen after surgery for congenital heart disease, particularly in
patients with Fontan-type operations and atrial switch
procedures for transposition of the great arteries [12]. Atrial
flutter is identified by so-called sawtooth waves representing
the rapid atrial rate with typically normal QRS duration.
Atrial fibrillation demonstrates chaotic irregular atrial
activity with an “irregularly irregular” ventricular rate;
QRS is usually normal in duration (Fig. 10).
Supraventricular tachycardia is one of the most common
arrhythmias encountered in pediatric patients (Fig. 11). The
term supraventricular tachycardia is confusing and does not
imply a single mechanism, however. Supraventricular
tachycardia includes any arrhythmia that requires atrial or
AV nodal tissue for their initiation and propagation, and
includes atrial tachycardias, atrial fibrillation, atrial flutter,
nodal tachycardia, junctional ectopic tachycardia, and others
[13] For the purposes of this discussion, SVT will be defined
as a paroxysmal tachyarrhythmia manifested by the absence
of P waves and by the presence of normal QRS complexes.
In children, there are 2 common mechanisms of SVT [14].
Both involve reentry mechanisms. In AV nodal reentry
tachycardia the reentry mechanism involves the AV node,
and in AV reentry tachycardia reentry proceeds via an
accessory pathway near, but not including, the AV node. Two
mechanisms are often indistinguishable via ECG. Preexcita-
tion syndromes are more common in children with AV
reentry tachycardia and are discussed below. The treatment
of SVT involves vagal maneuvers, adenosine, and in rare
cases synchronized cardioversion and is discussed in further
detail elsewhere [15].
Two additional SVTs occasionally encountered in pedia-
trics include junctional ectopic tachycardia and permanent
junctional reciprocating tachycardia (Fig. 12). Junctional
ectopic tachycardia is a common and frequently hemodyna-
mically deleterious rhythm seen in postoperative patients and
is discussed in a subsequent article. Permanent junctional
reciprocating tachycardia is a chronic, incessant form of
tachycardia involving an accessory pathway that presents in
infants and is electrocardiographically manifested by a
Fig. 8 Sinus tachycardia detected on Holter monitoring of a 6-year-old girl with near syncope. The heart rate is regular at 157 bpm.
352 M. O’Connor et al.
6. prolonged R-P interval [16]. It frequently causes a cardio-
myopathy which responds to rate control, although achieve-
ment of normal sinus rhythm can be extremely difficult.
5. Abnormal QRS duration tachycardias
Tachycardias demonstrating prolonged QRS duration for
age imply a ventricular origin to the arrhythmia. Ventricular
arrhythmias also demonstrate “bizarre” QRS morphologies.
Ventricular arrhythmias are uncommon in children and
usually arise in the setting of severe electrolyte disarray,
ingestion, or rare inherited disorders of cardiac conduction.
Ventricular arrhythmias, however, are poorly tolerated
hemodynamically so prompt recognition and initiation of
therapy are vital.
Premature ventricular contractions (PVCs) are a frequent
finding in children and may be cause for concern in rare
cases (Fig. 13). They are manifested on the ECG by bizarrely
shaped, wide QRS complexes with the associated T wave
usually pointing in the opposite direction of the QRS
complex. A compensatory pause after the PVC will be seen.
Premature ventricular contractions of uniform morphology
are less concerning than those of multiple forms. Ventricular
tachycardia consists of 3 or more successive PVCs at a
regular rate of 120 to 180 bpm (Fig. 14). As in adults, it can
degenerate into ventricular fibrillation, a usually lethal
rhythm unless promptly treated. Several special conditions
associated with ventricular tachycardia in children should be
Fig. 10 Atrial flutter in a neonate without structural congenital heart disease. Note the rapid ventricular rate and distinctive flutter waves
seen best in leads aVR and aVF.
Fig. 9 Ectopic atrial tachycardia captured on Holter monitoring of a young girl. Note how the P waves are difficult to separate from the QRS
complex owing to the high heart rate.
353The pediatric ECG
7. mentioned. The Brugada syndrome is a rare, autosomal
dominant, and frequently lethal disorder associated with
bouts of ventricular tachycardia and sudden death. A peculiar
“saddle-form” ST-segment elevation in the right precordial
leads with a family history suggests the diagnosis [17].
Arrhythmogenic right ventricular dysplasia is another rare
inherited disorder causing ventricular tachycardia and
sudden death in affected individuals due to the replacement
Fig. 12 Narrow complex tachycardia in an 8-month-old infant presenting with feeding difficulties, poor weight gain, and cardiomyopathy.
Electrophysiologic study revealed the diagnosis of permanent junctional reciprocating tachycardia.
Fig. 11 Supraventricular tachycardia in a 10-year-old boy with palpitations and a rapid heart rate. Note the regular rate, narrow QRS
complex, and absence of P waves. The tachycardia resolved with intravenous adenosine. Final diagnosis was orthodromic reciprocating
tachycardia due to an accessory pathway.
354 M. O’Connor et al.
8. of right ventricular myocardium with fatty and fibrous tissue.
Patients with this disorder typically present after puberty
with ventricular tachycardia, and the interval ECG is notable
for a persistent juvenile pattern of T-wave inversion and a
widened QRS complex in right precordial leads.
6. Ventricular preexcitation syndromes
The term preexcitation refers to ventricular depolarization
that is earlier than expected. Preexcitation can occur via
either a reentry pathway or an accessory pathway [18]. In
either case, the potential for sustained and dangerous
tachycardia exists because the AV node no longer “protects”
the ventricles from excessively high atrial rates. The
electrocardiographic appearance of preexcitation (Fig. 15)
consists of (a) normal P-wave morphology and axis, (b)
shortened PR interval, (c) prolonged QRS complex with
initial “slurring” (delta wave), and (d) Q waves and T-wave
abnormalities in what is termed a pseudoinfarction pattern.
The most common syndrome associated with preexcitation
in children and adults is the Wolff-Parkinson-White (WPW)
syndrome. In patients with WPW, the most commonly
encountered arrhythmia is a paroxysmal reentry SVT.
Detection of the “WPW pattern” (ie, delta wave with a
Fig. 14 Unprovoked ventricular tachycardia from Holter monitoring in a 13-year-old adolescent girl with syncope.
Fig. 13 Multiple PVCs in a 17-year-old adolescent boy with a history of transposition of the great vessels after arterial switch procedure.
Note the bizarre, wide QRS complexes interspersed with QRS complexes of normal configuration.
355The pediatric ECG
9. prolonged QRS complex) in an asymptomatic child warrants
cardiology referral, although the actual risk of sudden death
in this population is likely quite low [19].
7. Tachycardias associated with a prolonged
QT interval
Evaluation of the QT interval is an essential aspect of
ECG interpretation. Norms for the corrected QT interval
have been published and were discussed in the previous
article of this series. Prolongation of the QT interval is often
asymptomatic but puts the patient at risk of ventricular
arrhythmias, the most common of which is torsades de
pointes. Torsades de pointes is a form of polymorphic
ventricular tachycardia that has the ECG appearance of
“twisting along a string.” Prolongation of the QT interval
can be due to a multitude of factors, congenital and
acquired. QT prolongation is associated with hypokalemia
and hypocalcemia; it is also seen with administration of
antiarrhythmic agents. Many medications are associated
Fig. 16 Prolonged QT interval in an 18-year-old adolescent girl with familial long QT syndrome and a history of cardiac arrest. The QT
interval calculated by Bazett's formula is 506 milliseconds.
Fig. 15 Delta waves seen in a child with WPW syndrome who presented with SVT; preexcitation did not manifest until the tachycardia
resolved.
356 M. O’Connor et al.
10. with QT prolongation as well, particularly antibiotics and
older antipsychotics.
Congenital forms of the long QT syndrome warrant
discussion in pediatric patients. Congenital long QT
syndrome is a cause of pediatric sudden death and has
been associated with sudden death during sleep, exercise,
and perhaps a small subset of infants dying of sudden infant
death syndrome [20]. The 2 most common inherited long QT
syndromes are known eponymously as the Romano-Ward
and Jervell/Lange-Nielsen syndromes and are caused by
known mutations in cardiac ion channels. Congenital long
QT syndrome is a common cause of sudden death
attributable to cardiac causes in children; in an international
registry of long QT patients, 8% died suddenly during 5 years
of follow-up [21]. Certainly, identification of a prolonged QT
interval in a pediatric patient warrants pediatric cardiology
referral and close follow-up (Fig. 16).
8. Toxicology
Children frequently present to EDs after ingestion of
medications or other toxins, unintentionally or otherwise.
Obtaining an ECG is an important aspect of evaluating these
patients. A number of agents cause QRS prolongation,
mainly via blockade of the sodium channels responsible for
depolarization during phase 0 of the myocardial action
potential. Examples of such agents include tricyclic
antidepressants, diphenhydramine, propanolol, hydroxy-
chloroquine, and many antiarrhythmic agents [22]. QRS
prolongation in the setting of sodium channel blockade,
when severe, may lead to asystole unless therapy with saline
or sodium bicarbonate is administered.
Tricyclic antidepressant ingestion warrants special
attention owing to the multitude of effects on the ECG
[23]. The ECG presentation of such toxicity is dependent
on the specific medication ingested as well as the ingested
dose. Tricyclic antidepressants have 4 important effects:
(1) inhibition of presynaptic neurotransmitter reuptake; (2)
α-adrenergic receptor blockade; (3) anticholinergic effects;
and (4) sodium channel blockade. Collectively, these can
lead to tachycardia, QRS prolongation, and QT prolonga-
tion (Fig. 17).
β-Blockers and calcium-channel blockers are commonly
used medications in adults that not infrequently are
unintentionally ingested by children. β-Blockers are phar-
macologically heterogeneous with each agent exerting
single or multiple effects at β1, β2, and α1 receptors. Some
β-blockers contain sodium-channel blocking ability and may
prolong the QRS interval. Sotalol, a class III antiarrhythmic
agent, contains potassium channel blocking ability and can
cause QT interval prolongation [24]. β1 Receptors, however,
located in the myocardium, are largely responsible for the
cardiovascular sequelae of β-blocker overdose. Electrocar-
diogram manifestations of ingestion generally include
bradycardia, various grades of AV block, and QRS complex
widening. [25].
Calcium channel blockers cause predictable but non-
specific changes in the ECG. Common changes include
hypotension, bradycardia, and AV blocks [26]. Because
many current formulations of calcium channel blockers are
of the extended-release variety, symptoms may be delayed
for up to several hours postingestion [27]. Another
consideration in evaluating calcium channel overdose is the
cardioselectivity of the agent. Older agents such as nifedipine
may exert a predominantly vascular effect at lower doses,
resulting in hypotension with reflex bradycardia. Newer
Fig. 17 Sinus tachycardia with widened QRS complex, deep S wave in lead I, and prominent R wave in lead aVr. This ECG was recorded in
a lethargic adolescent with tricyclic antidepressant ingestion.
357The pediatric ECG
11. agents such as verapamil or diltiazem may result in
bradycardia and conduction disturbances without hypoten-
sion. At sufficient doses, however, selectivity is lost.
In summary, arrhythmias in otherwise healthy children are
relatively uncommon in the pediatric population but prompt
recognition will prevent excess morbidity and mortality. The
incidence of arrhythmias in patients with a history of
congenital heart disease is markedly higher and the ECG
manifestations of such arrhythmias in this patient population
will be described in the next article of this series.
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