1) Antidromic atrioventricular reentrant tachycardia (AVRT) occurs in less than 10% of patients with Wolff-Parkinson-White syndrome and can be difficult to distinguish from ventricular tachycardia on ECG.
2) Electrophysiological testing is often required to make the distinction, looking at features such as the His-ventricular interval, the effect of atrial and ventricular pacing on the tachycardia, and the response to pharmacological interventions.
3) Diagnostic maneuvers like atrial extrastimulation that advances ventricular activation or termination of the tachycardia with ventricular pacing support the diagnosis of antidromic AVRT rather than ventricular tachycard
differentiating between supraventicular tachycardia and ventricular tachycardia in wide complex rhythm is always confusing and management is totally different. correct diagnosis will make dramatic difference in patient management.
Inferior lead pseudo-infarct Q waves are a common finding in the Wolff-Parkinson-White (WPW) syndrome.The characteristic Q wave-T wave vector discordance results from secondary repolarization changes due to altered ventricular activation. As a corollary, the presence of T wave inversion with inferior lead Q waves and a short PR interval is strongly suggestive, but not pathognomonic of inferior ischemia.
Case-1:
A 23 years old medical student presented with occasional palpitation, shortness of breath and chest discomfort. He had the following ECG.
A 53 years old gentleman presented with palpitations for last 5 hours. He is smoker, diabetic, dyslipidemic and hypertensive. He had exertional chest discomfort for last 5 years and did coronary angiogram 3 years back and CAG revealed TVD and advised for revascularization. But he refused and was irregular in medication and reluctant for life style modification. He came to emergency department with this ECG.
differentiating between supraventicular tachycardia and ventricular tachycardia in wide complex rhythm is always confusing and management is totally different. correct diagnosis will make dramatic difference in patient management.
Inferior lead pseudo-infarct Q waves are a common finding in the Wolff-Parkinson-White (WPW) syndrome.The characteristic Q wave-T wave vector discordance results from secondary repolarization changes due to altered ventricular activation. As a corollary, the presence of T wave inversion with inferior lead Q waves and a short PR interval is strongly suggestive, but not pathognomonic of inferior ischemia.
Case-1:
A 23 years old medical student presented with occasional palpitation, shortness of breath and chest discomfort. He had the following ECG.
A 53 years old gentleman presented with palpitations for last 5 hours. He is smoker, diabetic, dyslipidemic and hypertensive. He had exertional chest discomfort for last 5 years and did coronary angiogram 3 years back and CAG revealed TVD and advised for revascularization. But he refused and was irregular in medication and reluctant for life style modification. He came to emergency department with this ECG.
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.
In cases of right atrial enlargement the duration of the P wave hardly changes, but the P-R interval increases, so that the P--R segment ratio falls below the normal range.Left atrial enlargement, on the other hand,does not affect the P-R interval, but the P wave lengthens at the expense of the P-R segment.The result is a- ratio above P-R segment the normal maximal limit of 1.6.In combined atrial enlargement, both P-R interval and P wave are prolonged. It follows that in such cases the ratio may P-R segment
be normal.
preop TEE assessment of atrial septal defect is very important for making decision for device closure, properly assessed adequate rims of ASD will reduce risk of device embolization to almost nil.
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.
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.
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.
In cases of right atrial enlargement the duration of the P wave hardly changes, but the P-R interval increases, so that the P--R segment ratio falls below the normal range.Left atrial enlargement, on the other hand,does not affect the P-R interval, but the P wave lengthens at the expense of the P-R segment.The result is a- ratio above P-R segment the normal maximal limit of 1.6.In combined atrial enlargement, both P-R interval and P wave are prolonged. It follows that in such cases the ratio may P-R segment
be normal.
preop TEE assessment of atrial septal defect is very important for making decision for device closure, properly assessed adequate rims of ASD will reduce risk of device embolization to almost nil.
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.
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.
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
Ventricular tachycardia are difficult to understand. it is classified in to two types. 1. VT in structurally normal heart, 2. VT in heart with structural diseases. I have tried to simplify the VT in structurally normal heart, which may be helpful to many students and learners.
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Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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.
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
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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
5. Antidromic AVRT clinically documented in ,5% of patients with WPW syndrome, and may be induced
in ,10% in the electrophysiology laboratory.
In adults, this usually happens in patients with multiple pathways or with free wall pathways located at
least .4 cm from the AV node, but in children it may be also seen with septal pathways.
Although patients with inducible antidromic tachycardia had accessory pathways with shorter ERPs
and there is an increased incidence of induced AF.
the occurrence of adverse events such as death or fast pre-excited AF within a mean follow-up of 6
years did not differ from patients without inducible antidromic tachycardia.
6. Prognostic Significance Of Inducible Antidromic AVRT
In children, it may represent an adverse prognostic sign.
This difference between children and adults might be related :-
Incidence of AVRT increases with age, but the tachycardia cycle length and antegrade refractory
period of the pathway also decreases , and one-third of patients may lose the WPW pattern at ages 30
– 70 years.
Induction of pre-excited tachycardia appears to be a surrogate marker of a more ‘aggressive’
accessory pathway.
Inducibility or clinical detection of antidromic AVRT may suggest an increased risk only in children.
In the adult population, the prognostic significance of pre-excited tachycardia is not established
7. ANTIDROMIC AVRT
Antidromic AVRT is the least common arrhythmia associated with Wolff-Parkinson-White
syndrome, occurring in less than 10 percent of patients.
As with orthodromic AVRT, antidromic AVRT can be initiated by atrial or ventricular premature
beats (APBs or VPB).
APBs initiating antidromic AVRT are blocked in the AV node/His-Purkinje system but conduct
antegrade to the ventricles over the accessory pathway.
After conduction through the ventricles, the impulse then travels back to the atria in a retrograde
fashion via the AV node/His-Purkinje system to complete the first reentrant loop.
VPBs initiating antidromic AVRT are blocked in the accessory pathway but conduct retrograde to
the atria over the AV node/His-Purkinje system. After conduction through the atria, the impulse
then travels back to the ventricles in an antegrade fashion via the accessory pathway to complete
the reentrant circuit.
8. ANTIDROMIC ATRIOVENTRICULAR REENTRANT TACHYCARDIA.
The initiation of classic antidromic AVRT by an AES requires the following:-
1) intact anterograde conduction over the BT
2) anterograde block in the AVN or HPS
3) intact retrograde conduction over the HPS-AVN once the AVN resumes
excitability following partial anterograde penetration .
retrograde conduction over the HPS-AVN is usually the limiting factor for the
initiation of antidromic AVRT.
A delay of more than 150 milliseconds between atrial insertion of the BT and
HB is probably required for the initiation of antidromic AVRT.
9.
10. ATRIAL ACTIVATION SEQUENCE. The initial site of atrial activation in classic antidromic AVRT is
consistent with retrograde conduction over the AVN. If the antidromic AVRT is using a second BT
retrograde conduction, then the atrial activation sequence will depend on the location of that BT.
ventricular activation precedes HB activation during classic antidromic AVRT. Therefore, during
preexcited SVT, a positive HV interval favors preexcited AVNRT over antidromic AVRT.
ATRIAL-VENTRICULAR RELATIONSHIP. Conduction time over classic (fast) BTs is approximately 30 to
120 milliseconds. Therefore, the PR is short and fixed, regardless of oscillations in the tachycardia CL
from whatever cause.
Similar to all types of AVRT, the A/V ratio is always equal to 1. If the SVT persists in the presence of
AV block, antidromic AVRT is excluded.
11. ECG findings in Antidromic AVRT
The ECG during antidromic AVRT typically shows the following:-
Ventricular rate ranging from 150 to 250 (or greater) beats per minute and usually regular.
Wide QRS complexes which are fully preexcited.
Inverted P waves with an RP interval that is usually more than one-half the tachycardia RR interval
and a short PR interval.
Constant RP interval regardless of the tachycardia cycle length.
Susceptibility to antidromic AVRT also appears to be dependent upon a transverse distance of at
least 4 cm between the bypass tract and the normal AV conduction system. Consequently, most
antidromic AVRTs use a left-sided accessory pathway as the antegrade route for conduction.
14. In some patients with antidromic AVRT and a left-sided accessory pathway, preexcitation may not be
apparent in sinus rhythm because the time for the atrial impulse to reach the atrial insertion of the
accessory pathway is longer than the time to reach the AV node.
A rare variant of antidromic AVRT can occur in patients with multiple accessory pathways when
anterograde conduction occurs over one accessory pathways and retrograde conduction returns to
the atrium via a second accessory pathway.
In such cases, the AV node is not necessary for maintenance of reentry.
The ECG during pathway-pathway tachycardia is indistinguishable from conventional antidromic
AVRT, and confirmation of the precise circuit usually requires mapping at electrophysiology study.
Approximately 10 percent of patients undergoing catheter ablation can be found to have multiple
accessory pathways .
15. Preexcited QRS Tachycardia
1. A Fib with AP
2. A Flu with AP: 250~300/min
3. Tachycardia with Mahaim fiber
4. Antidromic AVRT
5. Tachycardia using 2 Aps
6. AVNRT with bystander AP
18. Brugada algorithm for distinguishing ventricular tachycardia (VT) from supraventricular
tachycardia (SVT)
19. Negative concordance is strongly suggestive of VT
exception:SVT with LBBB aberrancy may demonstrate negative concordance
Positive concordance -also indicates VT
exception: antidromic AVRT with a left posterior accessory pathway
22. Differentiation between VT and preexcited SVT is particularly difficult, because ventricular activation
begins outside the normal intraventricular conduction system in both tachycardias.
As a result, algorithms for WCT, like QRS morphology criteria, tend to misclassify SVTs with preexcitation as
VT.
However, preexcitation is an uncommon cause of WCT, particularly if other factors, such as age and past
medical history,suggest another diagnosis.
23.
24. Brugada algorithm for distinguishing ventricular tachycardia ( VT ) from preexcited
supraventricular tachycardia (SVT )
The final
sensitivity and
specificity of
these three
consecutive
steps to
diagnose
ventricular
tachycardia
were 0.75 and
1.OO,
respectively.
26. Baseline Observations during Normal
Sinus Rhythm
The presence of preexcitation during NSR or atrial pacing suggests SVT, and the absence of
preexcitation during NSR and atrial pacing excludes preexcited SVT.
Induction of Tachycardia
The mode of induction cannot distinguish between SVT and VT. Both atrial and ventricular
stimulation may induce SVT or VT.
VTs that can be induced with atrial pacing include verapamil-sensitive VT, adenosine-sensitive VT,
and BBRVT.
27. Tachycardia Features
QRS MORPHOLOGY
when the QRS configuration of the WCT is not compatible with any known form of aberration,
the rhythm is likely to be VT or preexcited SVT.
QRS morphology during WCT that is identical to that during NSR may occur in SVT with BBB ,
preexcited SVT (when NSR is also fully preexcited), BBR VT, and interfascicular VT.
28. HIS BUNDLE–VENTRICULAR INTERVAL
When the His bundle–ventricular (HV) interval is positive (i.e.,the His potential precedes the QRS
onset), an HV interval during the WCT shorter than that during NSR (HVWCT < HVNSR) indicates
VT or preexcited SVT. In contrast, an HVWCT equal to or longer than HVNSR indicates SVT with
aberrancy, BBR VT.
When the HV interval is negative (i.e., the His potential follows the QRS onset), BBR VT and SVT
with aberrancy are excluded. However, myocardial VTs and preexcited SVT generally have negative
HV intervals.
Prolongation of the VA (and VH) interval and tachycardia cycle length (CL) with transient RBBB
(caused by catheter- induced trauma or introduction of a ventricular extrastimulus [VES]) is
diagnostic of antidromic AVRT using a right-sided.
29. OSCILLATION IN THE TACHYCARDIA CYCLE LENGTH
Variations in the tachycardia CL (the V-V intervals) that are dictated and preceded by similar
variations in the A-A or H-H intervals are suggestive of SVT with aberrancy or BBR VT.
variations in the V-V intervals that predict the subsequent H-H interval changes are
with myocardial VT or preexcited SVT.
HIS BUNDLE–RIGHT BUNDLE BRANCH POTENTIAL SEQUENCE
When both the HB and right bundle branch (RB) potentials are recorded,an HB-RB-V
activation sequence occurs in SVT with aberrancy and BBR VT with an LBBB pattern.
an RB-HB-V activation sequence occurs in antidromic AVRT using an atriofascicular or
right-sided BT, the uncommon type of BBR VT with RBBB pattern, or myocardial VT
originating in the RV.
RB-V-HB activation sequence occurs in antidromic AVRT using atriofascicular BT.
V-RB-HB or a V-HB-RB activation sequence can occur in VT.
30. Diagnostic Maneuvers During Tachycardia
ATRIAL EXTRASTIMULATION
Atrial extrastimulus (AES), regardless of its timing, that advances the next ventricular activation
with similar QRS morphology to that of the WCT excludes VT.
AES that delays the next ventricular activation excludes VT.
If the AES advances the next ventricular activation with similar QRS morphology as that of the
WCT, it proves that the BT is mediating ventricular activation during the WCT and that the WCT
is A preexcited SVT, and VT is excluded.
If the AES advances the timing of both the next ventricular activation and the subsequent atrial
activation, it proves that the SVT is an antidromic AVRT using an atrioventricular or
atriofascicular BT anterogradely, and excludes preexcited AVNRT and VT .
If the AES delays the next ventricular activation, it proves that the svt is an antidromic avrt using
an atrioventricular or atriofascicular BT anterogradely, and excludes preexcited AVNRT and VT
31. ATRIAL PACING
The ability to dissociate the atrium with rapid atrial pacing without influencing the
CL (V-V interval) or QRS morphology suggests VT and excludes preexcited SVTs, AT with
aberran cy,and orthodromic AVRT with aberrancy.
During VT, atrial overdrive pacing at a CL 20 to 60 milliseconds shorter than the tachycardia
CL with 1:1 AV conduction results in anterograde capture with changing or narrowing of the
tachycardia QRS morphology.
During VT when the tachycardia resumes after cessation of pacing, the earliest occurs in the
ventricle because the atrium is being passively driven by the ventricle during the
This results in a “V-V-A response.” On the contrary,
during antidromic AVRT or aberrantly conducted SVT, anterograde conduction occurs over
BT or AVN; and on cessation of atrial pacing, the last reset ventricular activation conducts to
the atrium over the retrograde limb of the circuit, resulting in a “V-A response” and
continuation of the tachycardia.
32. VENTRICULAR PACING
Antidromic AVRT usually can be terminated by ventricular pacing.
Termination occurs by retrograde invasion and concealment in the BT,resulting in anterograde
block over the BT following conduction to the atrium through the AVN.
33. TERMINATION AND RESPONSE TO PHYSIOLOGICAL AND PHARMACOLOGICAL
MANEUVERS
Carotid sinus massage and adenosine terminate classic antidromic AVRT after ventricular
activation, secondary to retrograde block up the AVN.
Preexcited typical AVNRT terminates after atrial activation, secondary to anterograde block
down the slow AVN pathway.
Termination or prolongation of the VA (and V-H) interval and tachycardia CL with transient
RBBB,caused by mechanical trauma or introduction of VES, is diagnostic of antidromic AVRT
using a right-sided or septal BT and excludes preexcited AVNRT.
Continuation of an SVT at the same tachycardia CL, despite anterograde block in the BT (by
drugs, mechanical trauma caused by catheter manipulation, or ablation), excludes antidromic
AVRT.