Wolff–Parkinson–White syndrome (WPW) is one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals travelling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supraventricular tachycardia referred to as an atrioventricular reciprocating tachycardia.The incidence of WPW is between 0.1% and 0.3% in the general population.Sudden cardiac death in people with WPW is rare (incidence of less than 0.6%), and is usually caused by the propagation of an atrial tachydysrhythmia (rapid and abnormal heart rate) to the ventricles by the abnormal accessory pathway.
Wolff–Parkinson–White syndrome (WPW) is one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals traveling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supra-ventricular tachycardia referred to as an atrio-ventricular reciprocating tachycardia.
AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of tachycardia (fast rhythm) of the heart. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medication, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node.
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
Wolff–Parkinson–White syndrome (WPW) is one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals traveling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supra-ventricular tachycardia referred to as an atrio-ventricular reciprocating tachycardia.
AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of tachycardia (fast rhythm) of the heart. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medication, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node.
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
Tachycardias are broadly categorized based upon the width of the QRS complex on the electrocardiogram (ECG). A narrow QRS complex (<120 milliseconds) reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the His bundle (ie, a supraventricular tachycardia). The site of origin may be in the sinus node, the atria, the atrioventricular (AV) node, the His bundle, or some combination of these sites. A widened QRS (≥120 milliseconds) occurs when ventricular activation is abnormally slow. The most common reason that a QRS is widened is because the arrhythmia originates below the His bundle in the bundle branches, Purkinje fibers, or ventricular myocardium (eg, ventricular tachycardia). Alternatively, a supraventricular arrhythmia can produce a widened QRS if there are either pre-existing or rate-related abnormalities within the His-Purkinje system (eg, supraventricular tachycardia with aberrancy), or if conduction occurs over an accessory pathway. Thus, wide QRS complex tachycardias may be either supraventricular or ventricular in origin.
Tachycardias are broadly categorized based upon the width of the QRS complex on the electrocardiogram (ECG). A narrow QRS complex (<120 milliseconds) reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the His bundle (ie, a supraventricular tachycardia). The site of origin may be in the sinus node, the atria, the atrioventricular (AV) node, the His bundle, or some combination of these sites. A widened QRS (≥120 milliseconds) occurs when ventricular activation is abnormally slow. The most common reason that a QRS is widened is because the arrhythmia originates below the His bundle in the bundle branches, Purkinje fibers, or ventricular myocardium (eg, ventricular tachycardia). Alternatively, a supraventricular arrhythmia can produce a widened QRS if there are either pre-existing or rate-related abnormalities within the His-Purkinje system (eg, supraventricular tachycardia with aberrancy), or if conduction occurs over an accessory pathway. Thus, wide QRS complex tachycardias may be either supraventricular or ventricular in origin.
Introduction to Electrophysiology - Supraventricular Tachycardias (1/4 lectures)Jose Osorio
What is cardiac Electrophysiology?
This presentation will cover basics of EP. It is Part 1 of 4 lectures about EP.
Part 1 - basics of EP and Supraventricular Tachycardias (SVT)
Part 2 - Ventricular arrhythmias and Cardiac Devices
Part 3 - Afib
Part 4 - EKG
ECG localization of accessory pathways slideshareCardiology
This presentation is simplified view of accessory pathways in heart and their localization with help of algorithms and ECG examples. Try to read this PPT in power point to see full effects and animations.
Pre-excitation Syndromes is a group of ECG and Electrophysiological abnormalities in which
The atrial impulses are conducted partly or completely, PREMATURELY, to the ventricles via a mechanism other than the normal AV-node *
Associated with a wide array of tachycardias with both normal QRS and prolonged QRS durations
Ohnell described this phenomenon as the “concertina
effect,” in which the QRS complex morphologies from individual
patients with WPW pattern differ owing to variation in the degree
of ventricular excitation via the accessory pathway and AV node.
Recognizing the concertina effect in WPW pattern as normal
variation is important to prevent unnecessary diagnostic and
therapeutic interventions.
Wellens syndrome. Wellens syndrome (also referred to as LAD coronary T-wave syndrome) refers to an ECG pattern specific for critical stenosis of the proximal left anterior descending artery. The anomalies described occur in patients with recent anginal chest pain, and do not have chest pain when the ECG is recorded.
Congenital defects can put a strain on the heart, causing it to work harder. To stop your heart from getting weaker with this extra work, your doctor may try to treat you with medications. They are aimed at easing the burden on the heart muscle. You need to control your blood pressure if you have any type of heart problem.
Changing your lifestyle can help control and manage high blood pressure. Your health care provider may recommend that you make lifestyle changes including:
Eating a heart-healthy diet with less salt
Getting regular physical activity
Maintaining a healthy weight or losing weight
Limiting alcohol
Not smoking
Getting 7 to 9 hours of sleep daily
CRISPR technologies have progressed by leaps and bounds over the past decade, not only having a transformative effect on
biomedical research but also yielding new therapies that are poised to enter the clinic. In this review, I give an overview of (i)
the various CRISPR DNA-editing technologies, including standard nuclease gene editing, base editing, prime editing, and epigenome editing, (ii) their impact on cardiovascular basic science research, including animal models, human pluripotent stem
cell models, and functional screens, and (iii) emerging therapeutic applications for patients with cardiovascular diseases, focusing on the examples of Hypercholesterolemia, transthyretin amyloidosis, and Duchenne muscular dystrophy.
A post-splenectomy patient suffers from frequent infections due to capsulated bacteria like Streptococcus
pneumoniae, Hemophilus influenzae, and Neisseria meningitidis despite vaccination because of a lack of
memory B lymphocytes. Pacemaker implantation after splenectomy is less common. Our patient underwent
splenectomy for splenic rupture after a road traffic accident. He developed a complete heart block after
seven years, during which a dual-chamber pacemaker was implanted. However, he was operated on seven
times to treat the complication related to that pacemaker over a period of one year because of various
reasons, which have been shared in this case report. The clinical translation of this interesting observation
is that, though the pacemaker implantation procedure is a well-established procedure, the procedural
outcome is influenced by patient factors like the absence of a spleen, procedural factors like septic measures,
and device factors like the reuse of an already-used pacemaker or leads.
Transcatheter closure of patent ductus arteriosus (PDA) is feasible in low-birth-weight infants. A female baby was born prematurely with a birth weight of 924 g. She had a PDA measuring 3.7 mm. She was dependent on positive pressure ventilation for congestive heart failure in addition to the heart failure medications. She could not be discharged from the hospital even after 79 days of birth, and even though her weight reached 1.9 kg in the neonatal intensive care unit. We attempted to plug the PDA using an Amplatzer Piccolo Occluder, but the device failed to anchor. Then, the PDA was plugged using a 4-6 Amplatzer Duct Occluder using a 6-Fr sheath which was challenging.
Accidental misplacement of the limb lead electrodes is a common cause of ECG abnormality and may simulate pathology such as ectopic atrial rhythm, chamber enlargement or myocardial ischaemia and infarction
A Case of Device Closure of an Eccentric Atrial Septal Defect Using a Large D...Ramachandra Barik
Device closure of an eccentric atrial septal defect can be challenging and needs technical modifications to avoid unnecessary complications. Here, we present a case of a 45-year-old woman who underwent device closure of an eccentric defect with a large device. The patient developed pericardial effusion and left-sided pleural effusion due to injury to the junction of right atrium and superior vena cava because of the malalignment of the delivery sheath and left atrial disc before the device was pulled across the eccentric defect despite releasing the left atrial disc in the left atrium in place of the left pulmonary vein. These two serious complications were managed conservatively with close monitoring of the case during and after the procedure.
Trio of Rheumatic Mitral Stenosis, Right Posterior Septal Accessory Pathway a...Ramachandra Barik
A 57-year-old male presented with recurrent palpitations. He was diagnosed with rheumatic mitral stenosis, right posterior septal accessory pathway and atrial flutter. An electrophysiological study after percutaneous balloon mitral valvotomy showed that the palpitations were due to atrial flutter with right bundle branch aberrancy. The right posterior septal pathway was a bystander because it had a higher refractory period than the atrioventricular node.
Percutaneous balloon dilatation, first described by
Andreas Gruentzig in 1979, was initially performed
without the use of guidewires.1 The prototype
balloon catheter was developed as a double lumen
catheter (one lumen for pressure monitoring or
distal perfusion, the other lumen for balloon inflation/deflation) with a short fixed and atraumatic
guidewire at the tip. Indeed, initially the technique
involved advancing a rather rigid balloon catheter
freely without much torque control into a coronary
artery. Bends, tortuosities, angulations, bifurcations,
and eccentric lesions could hardly, if at all, be negotiated, resulting in a rather frustrating low procedural success rate whenever the initial limited
indications (proximal, short, concentric, noncalcified) were negated.2 Luck was almost as
important as expertise, not only for the operator,
but also for the patient. It is to the merit of
Simpson who, in 1982, introduced the novelty of
advancing the balloon catheter over a removable
guidewire, which had first been advanced in the
target vessel.3 This major technical improvement
resulted overnight in a notable increase in the procedural success rate. Guidewires have since evolved
into very sophisticated devices.
Optical coherence tomography-guided algorithm for percutaneous coronary intervention. Vessel diameter should be assessed using the external elastic lamina (EEL)-EEL diameter at the reference segments, and rounded down to select interventional devices (balloons, stents). If the EEL cannot be identified, luminal measures are used and rounded up to 0.5 mm larger for selection of the devices. Optical coherence tomography (OCT)-guided optimisation strategies post stent implantation per EEL-based diameter measurement and per lumen-based diameter measurement are shown. For instance, if the distal EEL-EEL diameter measures 3.2 mm×3.1 mm (i.e., the mean EEL-based diameter is 3.15 mm), this number is rounded down to the next available stent size and post-dilation balloon to be used at the distal segment. Thus, a 3.0 mm stent and non-compliant balloon diameter is selected. If the proximal EEL cannot be visualised, the mean lumen diameter should be used for device sizing. For instance, if the mean proximal lumen diameter measures 3.4 mm, this number is rounded up to the next available balloon diameter (within up to 0.5 mm larger) for post-dilation. MLA: minimal lumen area; MSA: minimal stent area;NC: non-compliant
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.
The Human Developmental Cell Atlas (HDCA) initiative, which is part of the Human Cell Atlas, aims to create a comprehensive reference map of cells during development. This will be critical to understanding normal organogenesis, the effect of mutations, environmental factors and infectious agents on human development, congenital and childhood disorders, and the cellular basis of ageing, cancer and regenerative medicine. Here we outline the HDCA initiative and the challenges of mapping and modelling human development using state-of-the-art technologies to create a reference atlas across gestation. Similar to the Human Genome Project, the HDCA will integrate the output from a growing community of scientists who are mapping human development into a unified atlas. We describe the early milestones that have been achieved and the use of human stem-cell-derived cultures, organoids and animal models to inform the HDCA, especially for prenatal tissues that are hard to acquire. Finally, we provide a roadmap towards a complete atlas of human development.
The treatment of patients with advanced acute heart failure is still challenging.
Intra-aortic balloon pump (IABP) has widely been used in the management of
patients with cardiogenic shock. However, according to international guidelines, its
routinary use in patients with cardiogenic shock is not recommended. This recommendation is derived from the results of the IABP-SHOCK II trial, which demonstrated
that IABP does not reduce all-cause mortality in patients with acute myocardial infarction and cardiogenic shock. The present position paper, released by the Italian
Association of Hospital Cardiologists, reviews the available data derived from clinical
studies. It also provides practical recommendations for the optimal use of IABP in
the treatment of cardiogenic shock and advanced acute heart failure.
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.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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
2. Historical perspectiveHistorical perspective
The earliest description of an accessory
pathway was reported by Stanley Kent in
1893 who suggested that impulses can
travel from the atrium to the ventricle
over a node-like structure other than the
atrioventricular (AV) node.
Cohn and Fraser reported the first case
of pre-excitation syndrome in 1913
3. In 1930, Louis Wolff,
Sir John Parkinson, and
Paul Dudley White
published a seminal
article describing 11
young patients who
suffered from attacks
of tachycardia
associated with an
electrocardiographic
pattern of bundle
branch block with a
short PR interval
4. Ohnell was the first to use the term
“pre-excitation,” whereas Seters
described the slurred initial component
of the QRS complex as a “delta” wave.
5. Curative therapy of WPW syndrome was
demonstrated in 1967 when Cobb et al
successfully ablated an accessory pathway
during open-hear surgery
The first successful catheter ablation of
an accessory pathway by delivering direct
current energy was reported by Morady
and Scheinman in 1984.
6. In 1987, Borggrefe et al. successfully
ablated a right-sided pathway by
delivering RF current. Radiofrequency
ablation of accessory pathways has
become a first line therapy and is
favoured over the medical treatment in
most of the patients.
7. INTRODUCTIONINTRODUCTION
Patients with pre-excitation syndromes
have an additional or accessory pathway,
which directly connects the atria and
ventricles.
In the Wolff-Parkinson-White pattern,
AV conduction through the bypass tract
results in earlier activation (preexcitation)
of the ventricles than if the impulse had
travelled through the AV node
8. Classic accessory pathway is the AV
bypass tract or bundle of kent in WPW
James fibres, AN tracts connect atrium to
distal AV node
Brechenmacher fibres(atrio- hisian tracts)
connect atrium to HIS bundle
Hisian -fascicular tracts(Mahaim fibres)
13. FrequencyFrequency
Delta waves detectable on an ECG have been
reported to be present in 0.15% to 0.25% of the
general population.
A higher prevalence of 0.55% has been reported in
first-degree relatives of patients with accessory
pathways. Wolff–Parkinson–White syndrome is more
commonly diagnosed in men than in women, although
this sex difference is not observed in children.
Among those with the Wolff–Parkinson–White
syndrome, 3.4 percent have first-degree relatives
with preexcitation.
The familial form is usually inherited as a mendelian
autosomal dominant trait
14. Inherited form of WPW syndrome
associated with familial hypertrophic
cardiomyopathy has been recently
described with the locus mapped to
chromosome 7q33.
15. The term Wolff-Parkinson-White
syndrome is used to describe individuals
with ventricular pre-excitation and
symptomatic tachycardias as originally
described by Wolff, Parkinson and White.
The term Wolff-Parkinson-White pattern
refers to the electrocardiographical
finding of ventricular preexcitation.
16. VariantsVariants
Concealed Accessory Pathways
Defined as pathways that are capable of conduction only in
the retrograde (VA) direction at rates similar or greater than
the sinus rate.
The concealed accessory pathways are noted in between
15% to 42% of patients with accessory pathway.
Approximately one third of AVRTs are due to concealed
accessory pathways.
The clinical presentation of patients who have a concealed
accessory pathway is similar to the classic presentation of
WPW syndrome with the exception that no preexcitation,
rapid preexcited responses are not observed during AF.
Concealed pathways are more frequently localized to the left
free wall (64%), and less frequently in Septal (31%) and right
free wall locations.
17.
18. Decremental AccessoryDecremental Accessory
pathwayspathways
The electrophysiologic properties of
accessory pathways are similar to
working myocardium.
Few accessory pathways may exhibit
progressive delay in conduction in
response to increased rate of pacing.
Decremental conduction can be seen in
approximately 7% of the patients with
WPW syndrome
19. Multiple accessory pathways are present
in as many as 13 percent of patients
Most patients with accessory pathways
do not have any structural cardiac
abnormalities but as many as 10 percent
of patients with Ebstein’s anomaly have
one or more accessory pathways.
20. PathophysiologyPathophysiology
Accessory AV muscle bridges are normally
presented in human fetal hearts but these
connections are interrupted during growth
of the fibrous annulus
Most accessory pathways consist of small
fibers resembling ordinary myocardium
crossing the AV groove.
The pathways insert directly into the atrial
and basal ventricular myocardium but they
may course through the AV groove at
variable depth ranging from subepicardial to
subendocardial locations.
21. Accessory pathways may have an oblique
course rather than perpendicular to the
transverse plane of the AV groove,
resulting in an atrial insertion that may be
transverse some distance from the
ventricular insertion site.
22. The presence of very short AV nodal
conduction times may cause the ventricular
preexcitation to be invisible on the surface
ECG.
Preexcitation can also be minimal when the
accessory pathway is located on the lateral
mitral ring relatively far from the origin of
the sinus impulse.
It was postulated that preexcitation pattern
with a PR interval >120ms typically indicates
a left free wall accessory pathway.
23. AV reentrant tachycardias (AVRT) occur
when two functionally different
conduction pathways are present.
The effective refractory period of the
accessory tract is usually longer than that
of the normal AV nodal His-Purkinje
tract.
29. Patients with antidromic tachycardias have
usually shorter refractoriness in the normal
retrograde VA conduction system and the
maintenance of tachycardia is favored by the
greater distance from the normal AV node.
AVRT using two accessory pathways is a
rare form of tachycardia with broad QRS
complexes in which anterograde conduction
is down one accessory pathway and
retrograde conduction is up another.
30. The rate of the AVRT depends on the
conduction times of all tissues involved in
the reentrant circuit and on the
autonomic tone modulation.
QRS complex alternans during
supraventricular tachycardia is relatively
specific for AVRT.
31. AFAF
Ventricular rates up to 350 bpm are
possible and the QRS morphology
reflects varying degree of preexcitation
due to conduction over the normal AV
node as well as the accessory pathway.
A causal relationship between ventricular
fibrillation and atrial fibrillation with rapid
ventricular response has been
documented
32.
33.
34. SymptomsSymptoms
The usual complaint of patients with WPW
syndrome and recurrent tachycardia is
usually rapid palpitations associated with
chest discomfort, shortness of breath,
lightheadedness or syncope.
The onset and offset are typically sudden.
Some patients may report precipitating
factors such as coffee, stress, menstrual
periods or pregnancy but most usually the
symptoms are sporadic and unpredictable.
35. Sudden death is rare but may sporadically
be the initial presentation in previously
asymptomatic individuals.
A history of syncope raises concerns
regarding a very rapid arrhythmia with
haemodynamic compromise.
36. The WPW pattern in symptomatic or
asymptomatic infants usually disappears,
especially in the first year of life.
However, once symptomatic recurrent
tachycardias appear in adolescence or
adulthood, the course is usually one of
recurring episodes.
37. Sudden death in WPWSudden death in WPW
syndromesyndrome
The incidence of sudden cardiac death in patients
with the WPW syndrome has been estimated to
range from 0.15% to 0.39%.
It is unusual for cardiac arrest to be the first
symptomatic manifestation of WPW syndrome.
Risk factors identified for sudden death include,a
shortest pre-excited R-R interval less than 250ms
during spontaneous or induced AF, history of
symptomatic tachycardia, multiple accessory
pathways, Ebstein’s anomaly and familial WPW
syndrome.
38. Findings suggestive of a low likelihood of
sudden death include
preexcitation that is intermittent,
the ability to produce anterograde
conduction block with drugs such as
procainamide, and
the disappearance of preexcitation during
exercise
39. In patients without manifest pre-excitation
the initial activation of the septum is usually
from the left to the right side producing a Q
wave in lateral leads and R wave in lead aVR.
It was claimed that in the presence of a
manifest accessory pathway the usual septal
activation is masked and therefore the
finding of a septal Q wave in lead excludes
ventricular pre-excitation.
However, several other studies have
reported the presence of the septal Q wave
in lead V6 despite manifest pre-excitation.
40.
41.
42. 46 to 60 percent of
accessory pathways are
found within the left free
wall space
25 percent are within
the posteroseptal space
13 to 21 percent of
pathways are within the
right free wall space
2 percent are within the
anteroseptal space
AV ACCESSORY PATHWAYSAV ACCESSORY PATHWAYS
43. Localization of the accessoryLocalization of the accessory
pathwaypathway
Several algorithms have been proposed
for anatomical localization of the
accessory pathway.
Rosebaum in 1945 divided WPW into
type A, left sided pathways (tall R wave in
lead V1, i.e. a positive delta wave), and
type B, right sided pathways (QS
complex in lead V1, i.e. a negative delta
wave)
44.
45.
46. Polarity of QRS QRS
AXIS
DELT
A
AXIS
V1 V2 V3
Antero septal
- - - NORMAL NORMAL
Rt lat
- - - LEFT
[ -60]
LEFT
[ -60]
Rt postseptal
- + + LEFT [ -30] LEFT[ -60]
Lt postseptal
+ + + LEFT[ -30] LEFT[ -60]
47. DELTA IN
V1
QRS IN V1 QRS IN V2
RT POST
SEPTAL
ISO or NEGATIVE DOMINANTLY
NEGATIVE
POSITIVE
LT POST
SEPTAL
POSITVE
[ALWAYS]
DOMINANTLY
POSITIVE or
equiphasic
positive
48.
49. The predictive accuracy of all these
algorithms is significantly reduced in the
presence of multiple pathways.
Coexistent anomalies such as Acute MI
or LVH may alter the QRS morphology
50. ElectrophysiologicalElectrophysiological
assessmentassessment
The main indication for electrophysiological
testing is a decision to undergo catheter ablation
or less frequently, diagnostic study for risk
stratification.
Electrophysiological studies utilize the placement
of a decapolar catheter to the coronary sinus and
three quadripolar catheters to the high right
atrium, right ventricular apex and His bundle
region.
The presence of an accessory AV connection is
confirmed by the presence of a delta wave on the
surface ECG and increased preexcitation and
shortening of HV interval during incremental and
programmed atrial pacing.
51. Indications ofIndications of ElectrophysiologicalElectrophysiological
Studies in WPWStudies in WPW
1) Sudden deaths have the peculiarity to occur during
exercise, hence all competitive athletes with WPW
syndrome should be studied.
2) Patient with high responsibility profession such as
professional pilot (plane, truck, bus, train)
3) The indications in children are more controversial, the
conductionin accessory pathway and normal AV conduction
system are more rapid, probably without a clinical
significance.
The indications should be liberal in children who are
competitive athletes and in all children above the age of 10
years.
4) In elderly, the propensity for atrial fibrillation increases
hence the risk of occurrence of a potentially severe
arrhythmia in an asymptomatic WPW patient should not be
underestimated.
52. Atrial pacing from the sites closer to the
accessory pathway will preferentially
conduct over this pathway with enhanced
preexcitation.
Therefore, in a patient with a left-sided
accessory pathway, the stimulus to delta
wave will be shorter during pacing from the
coronary sinus than during right atrial
pacing. This is especially useful in exposing
left-sided pathways with minimal
preexcitation on the surface ECG.
53. Multipolar catheters located in the coronary
sinus are useful for accurate localization of
the left sided accessory pathways as the
coronary sinus runs in the epicardial fat in
the posterior groove around the posterior
and lateral aspects of the mitral valve.
The coronary sinus ostium empties into the
junction of the inferior and medial walls of
the right atrium and approximates the
inferoposterior corner of the interatrial
septum.
54. Mapping on the tricuspid ring is more
difficult and preformed sheaths to facilitate
contact, multipolar “halo” catheters to
record signals along the tricuspid ring or
catheters for mapping within the right
coronary artery are available.
The distal portion of the catheter recording
the His bundle electrogram approximates
the superior limit of the atrial septum where
it joins the tricuspid valve.
55. Exact localization of an accessory pathway
may be limited by the possible occurrence of
multiple pathways.
It may also be difficult to distinguish
between retrograde atrial activation due to
a midseptal pathway and atypical AV node
reentry.
The use of pharmacologic agent that
selectively slows conduction over the AV
node, such as adenosine, may be useful to
accentuate accessory pathway conduction
during atrial pacing.
61. Antidromic tachycardiaAntidromic tachycardia
Obligatory 1:1 AV relationship.
QRS morphology in tachycardia consistent
with max preexitation.
Tachycardia QRS morphology reproduced
by atrial pacing near pathway insertion.
Advanced ventricular activation by atrial
extrastimuli near insertion with
advancement of subsequent His activation.
Changes in V –His interval precede changes
in cycle length.
62. The presence of an accessory pathway
participating in the tachycardia circuit can
be confirmed by prolongation of the cycle
length with ipsilateral bundle branch
block and termination of tachycardia
after a premature ventricular
extrastimulus that does not conduct to
the atria and occurs when the His bundle
is refractory.
63.
64. Differentiation between atrial tachycardia
and AVRT is best accomplished by
dissociating the ventricles from the
tachycardia.
The demonstration of a VA-AV response
after termination of ventricular pacing
that entrains the atrium excludes an
AVRT and confirms atrial tachycardia
65. For left free wall accessory pathways, the
diagnosis of AVRT can be mimicked by
antrioventricular nodal reentry with
eccentric atrial activation or by atrial
tachycardias arising from the CS
musculature or the ligament of Marshall.
66. The differential diagnosis of an antidromic
tachycardia includes ventricular tachycardia that
should be diagnosed by the dissociation of the
atrium from the ventricle or a variable His-to-
atrium timing relationship without alteration of
the tachycardia cycle length.
Antidromic tachycardia is diagnosed by
demonstrating the reproduction of tachycardia
QRS morphology by atrial pacing at the
presumed accessory pathway insertion site and
advancement of the ventricular and subsequent
His activation by a premature atrial stimulus near
the accessory pathway site.
67. VA conduction indices : Using
ventricular-induced atrial pre-excitation,
Miles et al devised pre-excitation index
Progressively premature right ventricular
extrastimuli were introduced during
tachycardia and the difference between
the TCL and the longest stimulation
interval at which atrial pre-excitation
occurred
pre-excitation indexpre-excitation index
68.
69. Atrial preexcitation at >90% TCL means
the presence of a septal or right sided BT
If PEI is <25 then Anteroseptal or Right
Free Wall
If PEI is > 75 then Left Lateral or AVNRT
70. More than 75 ms – left free wall
Less than 45 ms- septal tracts
71. The new index was computed
(AV conduction time during SVT) +
(ventriculoatrial conduction time during
ventricular pacing at the SVT cycle length)
-(SVT cycle length).
72. new index could differentiate AV
reentrant tachycardia (index 60 ms,)
from AV nodal reentrant tachycardia
( 100 ms ).
Editor's Notes
Figure 2. Image of preexcitation of the EKG with a manifest accessory pathway leading to the EKG findings of WPW pattern. As seen here, electrical conduction from the atria to the ventricles can occur via the normal AV nodal system and the accessory pathway simultaneously. This leads to the creation of the slurred upstroke, or delta wave, seen on the surface EKG lead and denoted by arrows in the tracing seen here. -- Figure 2. Image of preexcitation of the EKG with a manifest accessory pathway leading to the EKG findings of WPW pattern. As seen here, electrical conduction from the atria to the ventricles can occur via the normal AV nodal system and the accessory pathway simultaneously. This leads to the creation of the slurred upstroke, or delta wave, seen on the surface EKG lead and denoted by arrows in the tracing seen here. -- Image of preexcitation of the EKG with a manifest accessory pathway leading to the EKG findings of WPW pattern. As seen here, electrical conduction from the atria to the ventricles can occur via the normal AV nodal system and the accessory pathway simultaneously. This leads to the creation of the slurred upstroke, or delta wave, seen on the surface EKG lead and denoted by arrows in the tracing seen here.
One beat from a rhythm strip demonstrating characteristic ECG features of the Wolff-Parkinson-White syndrome. Note the short PR interval, delta wave and prolonged QRS complex.
Illustration of orthodromic atrioventricular reciprocating tachycardia (AVRT) with a reentrant circuit consisting of 2 limbs. The forward or antegrade limb involves the normal AV nodal system, and the reverse, or retrograde, limb involves the accessory pathway. This type of SVT leads to a narrow-complex rhythm on the EKG as seen above. Illustration of orthodromic atrioventricular reciprocating tachycardia (AVRT) with a reentrant circuit consisting of 2 limbs. The forward or antegrade limb involves the normal AV nodal system, and the reverse, or retrograde, limb involves the accessory pathway. This type of SVT leads to a narrow-complex rhythm on the EKG as seen above. ortho
anti
Figure 17. A: Septal depolarisation in patients without manifest pre-excitation producing a septal R wave in lead aVR). B: Depolarisation of the myocardium through the accessory pathway manifested by a negative delta wave in lead aVR.
Magnification of surface electrographic lead V6. There is an RSR’ pattern before (A) and QR pattern after (B) successful ablation of a left lateral accessory pathway. It would not be very difficult to miss the first positive deflection on the left hand side picture and misinterpret the S wave as a Q wave.
ARUDA
Figure 5. Stepwise algorithm for the prediction of accessory pathway localization using a 12 lead ECG. The main criteria considered in the algorithm were horizontal QRS transition, R/S relationship in leads I and aVL, delta wave polarity and frontal axis and R wave amplitude in lead III. Fitzpatrick proposed a stepwise algorithm for the localization of accessory pathway (Figure 5)45.
Figure 7. Occurrence of left bundle branch block during AVRT. A. AVRT without functional bundle block. B. The development of left bundle branch block is associated with the prolongation of the VA interval and the tachycardia cycle length indicating utilization of a left lateral accessory pathway as the retrograde limb of this tachycardia circuit. V6 – ECG lead V6, AE – intracardiac electrogram from the high right atrium.
Figure 8. Tracings from the 12-lead ECG illustrating the principle of PR dispersion. Lead II has the least pre-excited QRS complex with the longest PR interval (180 ms) whereas lead V5 is the most pre-excited with the PR interval of 100 ms. Thus, the PR dispersion was calculated as 180 – 100 = 80 ms.