This document discusses techniques for localizing the site of origin of ventricular tachycardia based on electrocardiogram characteristics. It describes that right ventricular outflow tract tachycardias typically present with left bundle branch block morphology while left ventricular sites may present with either right or left bundle branch block depending on exit site. Specific leads are discussed that can provide clues about anterior vs posterior, septal vs free wall origin within the outflow tracts. Other areas like fascicles, papillary muscles and mitral/tricuspid annuli are also summarized.
Idiopathic VT refers to VT occurring in structurally normal hearts in the absence of myocardial scarring. Classification of monomorphic idiopathic VT includes outflow tract VT, fascicular VT, papillary muscle VT,annular VT, and miscellaneous (VT from the body of the RV and crux of
the heart). It is commonly seen in young patients and usually has a benign course. The 12-lead lectrocardiogram is critical in distinguishing the specific form and locations of idiopathic VT. Treatment options include medical therapy specific to the underlying mechanism of VT or catheter
ablation.
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.
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.
A lecture on the echocardiographic evaluation of hypertrophic cardiomyopathy. Starts with an overview of the topic then a systematic approach to diagnosis and then a differential diagnosis followed by take-home messages and conclusion.
Idiopathic VT refers to VT occurring in structurally normal hearts in the absence of myocardial scarring. Classification of monomorphic idiopathic VT includes outflow tract VT, fascicular VT, papillary muscle VT,annular VT, and miscellaneous (VT from the body of the RV and crux of
the heart). It is commonly seen in young patients and usually has a benign course. The 12-lead lectrocardiogram is critical in distinguishing the specific form and locations of idiopathic VT. Treatment options include medical therapy specific to the underlying mechanism of VT or catheter
ablation.
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.
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.
A lecture on the echocardiographic evaluation of hypertrophic cardiomyopathy. Starts with an overview of the topic then a systematic approach to diagnosis and then a differential diagnosis followed by take-home messages and conclusion.
An electrocardiogram (ECG or EKG) records the electrical signal from your heart to check for different heart conditions. Electrodes are placed on your chest to record your heart's electrical signals, which cause your heart to beat. The signals are shown as waves on an attached computer monitor or printer
Neonatal ECG part 2, includes Atrial and ventricular hypertrophy f/b conduction disturbances and AV conduction heart block f/b electrolyte abnormalities and there ECG changes.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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
2. • VT exit site -point from which rapidly
expanding endocardial systolic
activation occurred on the isopotential
map synchronous with or just prior (up
to 40 msec) to surface QRS onset.
3. • >>70–80% of idiopathic VTs or VPCs
originate from RVOT
4. General Considerations
1. Left ventricular free wall VT =RBBB
2. VT exiting from the interventricular septum or right
ventricle =LBBB
3. Septal exits =narrower QRS complexes
4. Basal sites - positive precordial concordance
5. negative concordance == apical sites of origin
5.
6. Anatomic Considerations
• anteroseptal aspect of
RVOT is located in close
proximity to the LV
epicardium, adjacent to
the AIV and the LAD.
• posteroseptal aspect
of RVOT is adjacent to
the region of the RCC,
• anterior septal surface is
adjacent to the anterior
margin of the RCC or the
medial aspect of
theLCC.
7. • Simultaneous mapping
on the posterior RVOT
and the anterior wall of
the LVOT should be
performed to identify
the true earliest site of
origin.
• The top of RVOT may
be crescent shaped,
with the posteroseptal
region directed
rightward and the
anteroseptal region
directed leftward
8. •anteroseptal aspect of RVOT is
located in close proximity to the
LV epicardium, adjacent to the
AIV and the LAD.
•The posteroseptal aspect of
RVOT is adjacent to the region of
the RCC, and the anterior septal
surface is adjacent to the anterior
margin of the RCC or the medial
aspect of the LCC
9. •RVOT tachycardia
– LBBB
– inferior axis (R waves in II,III,aVF)
– QS complexes in aVR and aVL.
•Lead V1 : negative (LBBB)
•posterior RVOT or origin near or above the pulmonic valve (left side
of the body) = initial R wave in lead V1.
•R wave in lead V1 : potential anatomic sites of origin
10. Anterior RVOT (1) : LBBB morphology
• (2), (3) : between the posterior RVOT and the anterior right coronary cusp
(RCC) of the aortic valve. A small but variable R wave is seen in lead V1.
• (4) : more posteriorly in the region of the left coronary cusp (LCC)/aortic mitral
continuity(AMC) /noncoronary cusp(NCC) characterized with a distinct R wave in
V1.
• Even more posterior and leftward origin (the posterior mitral annulus) : RBBB
morphology.
11. Lead I
•The focus near or above the pulmonic valve (leftward in the body): typically all
negative (QS complex)
•Origin on the right side of the RVOT (free wall): positive lead I
•Origin posterior portion of the RVOT : positive lead I
•Origin anterior portion of the RVOT : biphasic pattern
12. Leads aVR and aVL (Both leads are superior leads.)
•Outflow tract VT (right or left) in a superior location : negative (QS
complexes) deflections in aVL and aVR
•Peri-His bundle region in the RVOT (most rightward and inferior portion) :
lead aVL (a left-sided lead) becomes isoelectric or slightly positive, lead aVR
(a right-sided lead) remains negative
•Suprapulmonary VT (anatomic location of the site in the left side of the
body) : greater amplitude negatively in the aVL compared to aVR
13. • Leads II, III, and aVF
• All outflow tract arrhythmias show a positive deflection in leads II, III,
aVF.
• The ratio of positivity (R-wave amplitude) : a clue to the site of origin.
• Suprapulmonary valve arrhythmia : a taller R wave in lead III than in II.
(the anatomic leftward location of the PV and lead III being an inferior and
rightward lead)
14. Localisation
• LV or RV?
• VTs arising from the LV have a RBBB like
morphology because the LV is activated before the
RV.
• VTs arising on or adjacent to the LV septum can
have a LBBB morphology if VTs exit from the septum
to the RV.
• Similarly, most VTs arising from the RV will have a
LBBB-like morphology.
• The anterior aspect of the LVOT is closely located to
the posterior aspect of the RVOT and the ECG
morphologies are similar each other
15. • RV origin VT
• RVOT
• Para hisian
• TA
• PA
• VT arising from other sites like PPM.
16. • RVOT VT
• LBBB
• inferiorly directed axis
• deeply negative QS - leads aVL and aVR.
• Septal sites on the RVOT -- narrower LBBB with
earlier precordial transition (positive QRS by V3 or
earlier) and higher amplitudes in the inferior leads.
• Free wall sites -- later precordial transitions (≥V4),
with broader QRS complexes and notching in the
inferior leads
17. • Posterior sites in the RVOT - leftward initial vector
( positive QRS complex in limb lead I)
• Anterior sites -- isoelectric or negative, often
multiphasic, forces in lead I.
• majority of RVOT VT foci lie at the top of the RVOT
within a 1–2-cm craniocaudal band subjacent to the
pulmonic valve=negative QS pattern in lead aVL.
• Isoelectric or positive forces in aVL =more caudal site
of origin at the base of the RVOT, potentially adjacent
to the His bundle.
18.
19.
20. Parahisian
•lower R-wave amplitude (III, aVF)
•shorter QRS duration (II, III, aVF)
•Larger R-wave amplitude in leads I, V5, and V6
•a QS pattern in V1.
•close anatomical proximity of the aortic root
• may overlap with OT VT arising from the NCC or RCC
of the aortic valve
•no specific ECG criteria reliably differentiate these sites.
21. Tricuspid Annulus (TA)
•LBBB
•inferior axis
•Lead aVL =monophasic positive or multiphasic
and of low amplitude.
•Free wall of the valve ring off the septum-
similar configuration is seen but with notching in
the limb leads.
22. Pulmonary Artery
•sleeves of myocardium extending above the semilunar
valves
•Typical RVOT VT, sometimes with taller R waves in the
inferior leads.
•pulmonary trunk is a more leftward structure than the
infundibulum,
•earlier precordial transition
•deeper QS in aVL than in aVR.
23. • Increased R-wave amplitudes on the inferior leads in
PA VT
• Lead I polarity: QS (rS) pattern in the PA VT, whereas
RVOT VT shows an R(Rs) pattern
• Early precordial transition at V3.
• The R/S amplitude ratio on lead V2 was significantly
larger than that in the RVOT.
• The average aVL/aVR ratio of Q-wave amplitude is >1
in PA VT.
24. VT Arising from Other Sites of RV(PPM)
•LBBB
•inferior in septal PPM origin or superior in ant. & post. PPM
•QRS width: 160 msec
•Presence of a notch in V1–V6,
•R-wave pattern in V1 (rS, QS), and
•Transition point from a predominantly negative S wave to a positive
R-wave deflection in the precordial leads
•Transition in <V4 in septal > V4 in ant. & post. PPM origin.
25. LV Origin Idiopathic VT
• LVOT
• 15–25% of OT
LCC/RCC/NCC& AMC AIV/GCV
LCC RCC JN. SEPTO PARA HISIAN
Supra valvular Infra valvular Epicardial
26. • more common –LCC than the right, rarely arises from
the NCC,
• LCC
• earlier precordial transition with broader and taller R
waves in V1 or V2
• taller inferior R waves, an S wave in lead I
• characteristic absence of S waves in V5 and V6.
• R-wave duration of >50% of the total QRS duration or
an R/S ratio of more than 30% =LCC origin.
• Characteristic multiphasic notched pattern in V1 with
an M” or “W” pattern, presumably due to transseptal
activation after initial LV activation from the LCC.
27.
28. • RCC
• left bundle-type pattern
• broad small R wave in V2
• precordial transition generally at V3.
• NCC: no pathognomonic ECG pattern
• LCC/RCC junction
• significant overlap between this group
• multiphasic notched V1 pattern seen in standard LCC
foci
• QS morphology in lead V1 with notching on the
downward deflection with precordial transition at lead
V6
29. • LCC/RCC junction
• • QS morphology in
lead V1 with notching on
the downward deflection
• • precordial transition at
lead V3
• • presence of late
potentials in sinus
rhythm at the site of
successful ablation
30. • Monomorphic ventricular tachycardia with LBBB morphology and
an inferior axis : DDx of RVOT and ASC origin
31. • LBBB morphologies with
right inferior axis
• VT arising from the anterior
septal side of the RVOT, from
the right or left coronary
cusp, and from the
pulmonary artery.
• R-wave progression : LV or the
aortic cusp
• R waves in V1 and V2 and a
transition by lead V3
• Left-sided outflow tract VT,
• Later transitions at V3 and V4 :
RVOT or the pulmonary artery
32. Infravalvular
• basal LVOT VT = VT
arising from the AMC that
characteristically displays a
qR pattern in V1
VT originating further leftward across
the anterior mitral annulus : the R
wave in lead I diminishes and a
broad, positive R wave is seen in lead
V1.
33. • Result of the left fibrous trigone deflecting
initial electrical activation leftward
• Depending the position and extent of the
trigone, AMC VT may not display this ECG
signature and may instead have an RBBB
pattern with positive concordance and no late
precordial S waves.
• Early transition and longer intrinsicoid
deflection.
34. • Septal-parahisian sites. ECG features.
• LBBB configuration more akin to RV foci and have a
dominant R in lead I, usually with left inferior axis
• A QS pattern in lead V1 and R wave in lead aVL also
were observed more often in the His group than that in
the RVOT.
• Narrow QRS, and small r wave in LII,LIII, aVF.
37. • shortest RS interval
• Maximum deflection index (MDI: interval from
the earliest ventricular activation to the peak
of the largest amplitude deflection in any
precordial lead divided by the QRS duration)
• larger in epicardial VT.
38. 1. pseudodelta wave in any precordial leads of
RBBB VTs- time from the QRS onset to the
earliest rapid deflection of ≥34 ms.
2. delayed intrinsicoid deflection=time from
QRS onset to the peak of the R wave in V2
of ≥85 ms.
3. shortest RS interval= time from the first
ventricular activation to the nadir of the first S
wave in any precordial leads of ≥120 ms
39. • Precordial MDI= shortest time to maximal positive or
negative deflection in any precordial lead divided by
the QRS duration.
• cut-off value of 0.55 = epicardial foci and other OT
sites of origin
• “Pattern break,” R-wave regression/progression-
abrupt loss of R wave in V2 followed by resumption in
R waves from V3 to V6
40. • Valles et al. described a four-step algorithm for
identifying epicardial origin VT from basal superior
and lateral LV in the setting of nonischemic
cardiomyopathy using the presence of inferior q
waves, pseudo-delta ≥ 75 ms, MDI ≥ 0.59, and
presence of q wave in lead I.
•
41. VA from LV summit( AIV/GCV):
• LVS - triangular
portion of the
epicardial LVOT
bounded by the
bifurcation between
the LAD and the LCX
• transected laterally by
the great cardiac vein
(GCV) at its junction
with the anterior
interventricular vein
(AIV).
42. • RBBB
• transition zone: early in V2
• R-wave amplitude ratio in leads III to II:
• Qwave amplitude ratio in leads aVL to aVR: >1.1
• S wave in lead V6 all accurately predicted the site of
origin of the idiopathic VAs originating from the LV summit
• Accessible area/ ablation succesful from GCV/AIV
• When LV summit VAs exhibit a III/II amplitude ratio of > 1.25
and an aVL/aVR amplitude ratio of > 1.75, those VAs are
likely to require a pericardial approach for ablation
43. • VT Arising from Other LV Sites
• Mitral annulus:
• delta wave-like beginning of the QRS complex.
• MA is located in the posterior portion of the LV and anterior,
and anterolateral sites have more predominant occurrence
than posteromedial sites.
• RBBB
• Early transition in V2
• Long QRS duration
• Negative QRS complex in LI
44. • Late notching in the inferior leads or an S wave in lead I, which are
found usually in both anterolateral MA and posterior MA VT, may be
absent in anterior or posteroseptal MA VT
45. PPM
•RBBB
•refractoriness to verapamil and Na+ channel blockers
•tendency for VPCs rather than VT
•inducibility with exertion
• lack of inducibility with programmed ventricular or atrial stimulation
•earliest ventricular activation at the base or middle portion of the
LV PPM
• absence of highfrequency potentials at the site of origin
•requirement of high RF power to achieve longterm ablation
success
46. • Anterolateral PPM:
• VTs exhibit RBBB pattern and right inferior axis QRS
morphology with an early precordial transition, generally before
V1. qR or qr pattern in lead aVR and rS pattern in lead V6 (R/S
ratio < 1) are useful features to differentiate from other LV sites.
The mean QRS duration during VT or VPCs is 168 ms.
• (b)Posteromedial PPM. VT with a posterior PPM origin showed
RBBB and right or left superior axis QRS morphology.
• The mean QRS duration during VT was within 160 ms.
• Monophasic R and qR pattern predominate in lead I. R/S
amplitude ratio <1 in V6
47. • Crux:
• On the epicardial surface of
the heart.
• JN of MCV with CS
• Ecg
• LBBB
• Early transition
• Left superior axis
• MDI >0.55
• Q in LII,LIII,aVF.
48. Fascicular VT:
»LPF VT
»LAF VT
»USF VT
RBBB, left superior axis, RS in
V5,V6.
VTs exhibit an RBBB configuration
with right axis deviation
its narrow QRS complex with
normal or rightward axis
deviation
49.
50. • The steps to finding the exit site are:
• What is the bundle branch block (BBB)
configuration?
• What is the inferior lead QRS complex
polarity?
• What is the lead I QRS complex polarity?
• What is the lead aVL QRS complex polarity?
• What is the lead aVR QRS complex
polarity?
• Where is the R-wave transition point?
51.
52. Take Home Messages
•Anatomic relationship between RVOT and LVOT : RVOT is anterior and to
the left of the LVOT
•ECG recognition of outflow tract tachycardia location
•R wave in lead V1 : clue to the potential anatomic sites of origin
•Precordial QRS transition: RVOT vs LVOT (RCC, LCC)
•Lead I : right vs left side of RVOT site QRS width: free wall vs septum of
RVOT Leads aVR and aVL : peri-His bundle region and suprapulmonary
VT Leads II, III, and aVF: suprapulmonary VT
•R-wave duration index ≥50% and R/S ratio ≥30% in lead V1 or V2 :
LVOT (RCC, LCC)
•Precordial MDI >0.55, delayed pattern of initial QRS activation, pseudo-
delta wave : epicardial LV VT