The document discusses electrocardiogram (ECG) findings associated with cardiac chamber enlargement. It notes that while ECG is not very sensitive, it can provide clues about underlying heart conditions. Enlargement of cardiac chambers on ECG is seen through changes in wave morphology, amplitude, axis, and duration. Specific criteria are discussed to identify left and right atrial abnormalities as well as left and right ventricular hypertrophy on ECG. Limitations of ECG criteria in the presence of conduction abnormalities are also reviewed.
Biatrial enlargement is diagnosed when criteria for both right and left atrial enlargement are present on the same ECG.
The diagnosis of biatrial enlargement requires criteria for LAE and RAE to be met in either lead II, lead V1 or a combination of leads.
Non infarction Q waves
Precise guide for Allied Health Science Students especially cardiac specialty students, DGNM, B.Sc Nursing & M.Sc Nursing Students regarding Non Infarction Q waves
Repolarization ST wave Abnormalities
Precise guide for Allied Health Science Students especially cardiac specialty students, DGNM, B.Sc Nursing & M.Sc Nursing Students regarding Repolarization ST wave Abnormalities.
Biatrial enlargement is diagnosed when criteria for both right and left atrial enlargement are present on the same ECG.
The diagnosis of biatrial enlargement requires criteria for LAE and RAE to be met in either lead II, lead V1 or a combination of leads.
Non infarction Q waves
Precise guide for Allied Health Science Students especially cardiac specialty students, DGNM, B.Sc Nursing & M.Sc Nursing Students regarding Non Infarction Q waves
Repolarization ST wave Abnormalities
Precise guide for Allied Health Science Students especially cardiac specialty students, DGNM, B.Sc Nursing & M.Sc Nursing Students regarding Repolarization ST wave Abnormalities.
Speckle tracking echocardiography (STE) is an echocardiographic imaging technique that analyzes the motion of tissues in the heart by using the naturally occurring speckle pattern in the myocardium or blood when imaged by ultrasound.
Speckle tracking echocardiography (STE) is an echocardiographic imaging technique that analyzes the motion of tissues in the heart by using the naturally occurring speckle pattern in the myocardium or blood when imaged by ultrasound.
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
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.
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.
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
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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
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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.
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.
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.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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.
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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.
2. Role of ECG
• ECG is a simple, readily available and
inexpensive tool for the detection of cardiac
chamber enlargement
• Can provide useful clues or arouse suspicion of
underlying cardiac condition
• Most ECG criteria have low sensitivity but high
specificity
• Clinical correlates and prognostic significance
• Screening and population based studies
3. General Principles
Enlargement of a cardiac chamber may manifest
on the ECG as an alteration of:
Wave form morphology
Amplitude / voltage
Axis
Duration (widening)
These apply to both the P wave and QRS
complex
Atrial abnormality may suggest corresponding
ventricular hypertrophy
4. Fallacies / Limitations
Enlargement ? Hypertrophy ? Dilatation ?
Voltage criteria can vary significantly based
on
Age
Gender
Race
Habitus (chest wall thickness/ abnormalities)
Pulmonary / pericardial pathology
5. Atrial abnormalities
Atrial dilatation, hypertrophy, elevated atrial
pressure, impaired ventricular distensibility, and
delayed intraatrial conduction produce similar
changes on the ECG and cannot be
differentiated
As such, the terms left atrial abnormality and
right atrial abnormality are preferable to
left /right atrial enlargement,
P mitrale/congenitale/pulmonale
J Am Coll Cardiol 2009;53:992–1002
6. P Wave
P wave reflects atrial
depolarisation
Right atrial activation
begins first.
Proceeds from SAN in
inferior and anterior
direction and is
reflected by ascending
limb of P wave in
frontal plane leads.
7. Left atrial activation
begins 0.03 sec after
right atrial activation
Proceeds from high in
the IAS in a left,
inferior and posterior
direction
Constitutes distal half
or descending limb of P
wave.
8. Normal P wave
Lead II LeadV1
Duration in lead II is 0.08 – 0.1 sec max.
0.11 sec.
Amplitude in lead II: Usually 2mm, max.
2.5 mm
Usually biphasic
Initial positive deflection < 1.5mm
Terminal negative deflection not exceeding
1 mm in depth and < 0.03 sec in duration.
Duration of P wave inV1 is 0.05 – 0.08 sec.
9. P wave axis
P wave axis in frontal plane: +45 to +65
Always positive in lead I, II, aVF,V4-V6 and
negative in lead AVR.
10. LEFT ATRIAL ABNORMALITY
3 basic ECG changes:
1. Prolongation and delay of the terminal or
left atrial component of atrial activation
(bachmann’s bundle)
2. Increased posterior deviation of left atrial
vector.
3. Left axis deviation of mean manifest frontal
plane P wave axis.
11. Criteria for LAA
Ratio between the duration of the P wave in lead 2
and the PR segment of >1.6 (Marcuz index)
Leftward shift of the P wave axis less than 15-30 o
V1 - PTerminal force
(MORRIS index)
Lead II
12. Echocardiographic evaluation of ECG
criteria for LAA
CRITERIA SENSITIVITY SPECIFICITY
Terminal negative P in V1 >
0.04 mm-sec
83 80
Duration between peak of P
wave notches > 0.04 s
15 100
P wave duration>0.11 s 33 88
Ratio of P wave duration to PR
segment > 1.6
31 64
Amplitude of terminal –ve P
wave deflection in V1 > 0.1mv
60 93
Munuswamy K et al Am J Cardiol 1984;53:829.
13. Causes of LA abnormality
Valvular heart disease, mainly mitral and
aortic
Hypertensive heart disease
Cardiomyopathy (dilated / restrictive /
hypertrophic)
CAD
Constrictive pericarditis with AV groove
constriction (rare)
14. P mitrale
The term P mitrale refers to a P wave that is abnormally notched and
wide because this P wave is commonly seen in patients with mitral
valve disease, particularly mitral stenosis.
15. Right atrial abnormality
Total P-wave duration is usually normal
Peaked P waves with amplitudes in lead II >0.25 mV
(even a normal amplitude P wave if pointed )
LeadV1:
Prominent initial positivity of the P wave inV1 orV2
(>0.15 mV)
Initial area under curve >0.06 mm-sec
qR complex, namely a small q followed by a large R
wave, usually in tricuspid regurgitation
Low-amplitude (< 0.6 mV) QRS complexes in leadV1
with a threefold or greater increase in leadV2
16. Change in P axis:
In acquired heart disease (e.g. COPD), rightward
shift of the mean P wave axis to above +75
degrees – ‘P pulmonale’
In congenital heart disease, the axis is normal or
to left (-40 to +70 degrees) – ‘P congenitale’
17. Kaplan criteria
QRS axis > 90o
P amplitude inV2> 0.15mv
R/S > 1 inV1 in the absence of RBBB
Combined sensitivity of 49% with specificity
of 100%
Kaplan JD, Evans GT et al. J Am Coll Cardiol 1994; 23: 747-52
18. Causes of RAA
Congenital heart disease (Ebstein’s anomaly,
severe PS)
Tricuspid valve disease
Chronic cor pulmonale (COPD)
RAA is very uncommon in isolated ASD without
PH since mean RA pressure is usually normal
19. P Pulmonale
Tall, peaked (“gothic”) P wave in leads II, III, and aVF ,P axis > 70 degrees
No good overall correlation between P pulmonale and right atrial enlargement
Severity of COPD is more related to rightward P wave axis than to P wave amplitude
20. P Tricuspidale
P wave in the frontal leads is notched and the first
component is increased in amplitude and taller than
the second component- reflects biatrial
enlargement
21. Himalayan P waves
Giant P waves-classically described in ebstein’s anomaly, also reported in
Tricuspid atresia, combined tricuspid and pulmonic stenosis
Best seen in leads II, III, aVF andV1
22.
23. Pseudo-P pulmonale
Tall peaked P waves in inferior leads in absence of right atrial enlargement
Seen in hypertensive heart disease with/without heart failure
Actually reflects Left atrial enlargement due to increase in the later P-
wave forces without prolongation of atrial depolarisation
24. Pseudo-P pulmonale
D- Pseudo P pulmonale pattern in left atrial enlargement.
The amplitude of the left atrial component is increased without increase in duration
of left atrial depolarization.
C- P mitrale –
increase in the left
atrial component in
amplitude and
duration.
Associated intraatrial
Conduction defect
- prolongation of P
wave duration
25. ECG evaluation of RAA & LAA is facilitated by differing times of
initiation of activation and by the differing directions of spread.
RAA- initial
component
of the P wave
is enlarged
leading to an
increase in
the height
of P wave
without any
widening.
LAA,
P-wave
widening with
an M-shaped
P wave in
lead II and
an increased
P terminal
force inV1
RAA LAA
Summary – LAA & RAA
26. Biatrial enlargement
Large biphasic P wave inV1
initial component > 1.5 mm in height and
terminal component > 1 mm in depth and 0.04 sec in
duration.
A P wave amplitude of more than 2.5 mm and
duration of more than 0.12 sec in lead II.
The presence of a tall, peaked P wave (>1.5 mm)
in the right precordial lead and a wide, notched P
wave in the limb leads or left precordial leads (V5
andV6)
28. Atrial abnormality in AF
AF itself indicates possible dilatation of the
atria in most diseases
Coarse f waves in leadV1 (>1 mm) were
associated with radiological and anatomic
evidence of atrial enlargement
30. Factors affecting QRS
voltage
Age: QRS voltages decline with age.The
commonly used voltage criteria apply to
adults>35 yrs
Gender: women have slightly lower voltages
Race: Blacks have higher voltages, hispanics and
caucasians lower compared to whites
Body Habitus:
Large breasts insulating effect.
Obesity increases LV mass but also distance of heart
from the electrodes. So QRS voltage is unaffected
JACC 2009;53:992–1002
31. Mechanisms of ECG changes
Prolongation of action potential duration
Increased transmural activation time
Change in cardiac position with LV dilatation
Brody effect
Secondary ST-T chamges possibly due to
subendocardial ischemia ( the term ‘strain’ is
to be avoided)
33. Ventricular activation time
Indicator of transverse conduction time across
LV wall
Prolonged in LVH (normal <40ms in Left leads, <20ms in right leads)
34. Classification of LV enlargement
LV volume LV mass
Normal Abnormal
Comments
Normal
Normal Concentric
LVH
Abnormal
volume ≥
90ml/m2
Abnormal Isolated LV
volume
overload
Eccentric LVH
Comments Abnormal LV mass ≥ 131g/m2 in males, 108
g/m2 in females
Huwez FU, Pringle SD, Marcfarlane PW. Am J Cardiol 1992; 70: 687
35. Pressure / Systolic overload
Increase in magnitude of QRS deflection.
Attenuation of small initial q wave in left
oriented leads
Increase inVAT (>40ms)
Counterclockwise rotation of heart so that
the transition zone is shifted to right i.e. in
leadV3 orV2.
36. LVH with pressure overload
T wave inverted in left oriented leadsV5,V6, I,AVL and upright inV1,V2, AVR.
InvertedT wave - blunt apex, asymmetrical limb, the proximal limb is shallower
than distal limb.
Associated ST segment is minimally depressed with slight upward convexity.
37. LVH with diastolic overload
Deep and narrow Q waves in left oriented leadsV5,V6.
The tallT waves in left precardial leadsV5,V6 are symmetrical sharply
pointed.
ST segment inV5,V6 minimally elevated and concavity upwards.
38. Differentiating diastolic
overload of AR and MR
Diastolic overload of MR can be distinguished
by ECG from AR.
MR – Gaint LA will displace the heart forward,
QRS vector is less aligned withV1 and more
aligned withV6. Hence S wave in leadVI will
be attenuated.
In AR, the S wave inV1 is deep
40. Selected criteria
Sokolow Lyon criteria (1949):
S inV1 + R inV5/V6 > 3.5 mv or
R inV5 orV6 > 2.6O mv.
Cornell voltage criteria (1987):
R in aVL + S inV3 > 2.80 mv for Males
> 2.00 mv for Females
41. Selected criteria
Cornell voltage-duration product
QRS duration × Cornell voltage > 244 mVms
QRS duration × sum of voltages in all leads
>1742 mm-sec
R in aVL > 11 mm.
R I + S III > 25 mm.
Total 12 lead voltage >175 mm
R-V6 > R-V5: Koito spodick criterion
QTc interval combined with CVP
44. LVH in the presence of
conduction disorders: RBBB
RBBB: reduces the S wave in the right precordial
leads (V1,V2) and thus reduces the sensitivity of
ECG for LVH
Presence of LAA & LAD enhance possibility of
LVH
45. LVH in the presence of
conduction disorders: LAFB
LAFB: QRS vector shifts in a posterior and
superior direction, resulting in larger R waves
in leads I and aVL and smaller R waves but
deeper S waves in leadsV5 andV6
46. LVH in the presence of
conduction disorders: LBBB
LVH and LBBB share a number of common
features like prolonged QRS duration and
voltage.
Criteria for LVH are most unreliable in the
presence of LBBB
LBBB itself is indicative of LVH in most cases
KLEIN et al, using echocardiograms, found that
in the presence of LBBB
SV2 + RV6 >45mm.
E/o LAE with QRS duration>0.16s
47. Significance
LVH on ECG correlated with increased CV
mortality
LIFE study showed improvement in survial
with LVH regression (Cornell criterion), also
HOPE trial (Sokolow Lyon criteria)
Secondary ST-T changes and associated LAE
indicate worse prognosis
48. Prominent STT changes in apical
hypertrophy (Yamaguchi syndrome)
Cornell product is one of the best predictors
of overall outcome
49. Right ventricular hypertrophy
The right ventricle is considerably smaller than
the left ventricle.
For RV forces to be manifested on the ECG, they
must be severe enough to overcome the
concealing effects of the larger LV forces.
In mild RVH, the ECG may be normal or there
may only be a shift of QRS axis.
50. ECG criteria for RVH
The ECG is notoriously inadequate in
detecting RVH
Its sensitivity is in the range of 2%–18% but it
is very specific (90%)
51. Vectorial classification of RVH (Chou and
Helm, 1967)
Type A: R inV1, S inV6 (CCW loop) - PS
Type B: R/S>1 inV1 with R> 0.5mV (CW loop) – RHD
MS
Type C: S inV5-6. with R/S<1 inV5, CW loop - COPD
52. RVH with pressure overload
Leads aVR,V1, andV2 – abnormally tall R waves.
I,aVL,V5,V6 – Deep S waves leading to RS or rS complex
Right axis deviation
54. Selected criteria
Sokolow-Lyon criteria : R inV1 + S inV5/V6 >
1.10 mV
R inV1 ≥ 0.7 mV
S wave inV5 orV6 >0.7 mV
qR inV1
R/S ratio inV1 > 1 with R >0.5 mV
R/S ratio of < 1 inV5 orV6
SI SII SIII syndrome
55. BUTLER LEGGETT FORMULA
Direction ANTERIOR RIGHT POSTERIOR-
LEFTWARD
Amplitude Tallest R or
R’ in V1/V2
Deepest S in
I or V6
S in V1
RVH formula A + R - PL > 0.7mv
56. Criterion for RVH Sensitivity (%) Specificity (%)
R inV1 ≥ 0.7 mV <10 —
QR inV1 <10 —
R/S inV1 > 1 with R > 0.5
mV
<25 89
R/S inV5 orV6 < 1 <10 —
S inV5 orV6 > 0.7 mV <17 93
57. Right axis deviation ≥ + 90 degrees <14 99
S1Q3 pattern <11 93
S1S2S3 pattern <10 —
P pulmonale <11 97
Murphy ML,Thenabadu PN, de Soyza N, et al: Reevaluation of electrocardiographic criteria for
left, right and combined cardiac ventricular hypertrophy. Am J Cardiol 53:1140, 1984.
Criterion for RVH Sensitivity (%) Specificity (%)
59. RVH with systolic overload
leadV1 –tall monophasic R wave or a diphasic RS, Rs, or qR complex.
T inversion in right precordial leads (‘strain’)
rS pattern inV6
In pure valvular PS, age 2-20, height of R wave in mm multiplied by 5
gives RV systolic pressure
60. RVH with RBBB
Pattern of incomplete or complete RBBB
RVH is present if R' in the precordial leads is greater than 10 mm in height in
incomplete RBBB, and 15 mm in complete RBBB- Barker &Valencia criteria
Incomplete
RBBB
61. Other Causes of tall R wave in
V1
Normal young adults
True posterior infarction
Dextrocardia
LPFB
Displacement of the heart due to pulmonary
disease
Wolff-Parkinson-White pattern
Muscular dystrophies
62. Sinus tachycardia
SI QIIITIII
Recent axis shift
“P pulmonale”
Complete or incomplete RBBB
NegativeT waves in two or more right precordial
leads
Clockwise rotation
Atrial arrhythmias
May mimic inferior wall MI or rarely anterior MI
Acute Pulmonary embolism
63.
64. BIVENTRICULAR HYPERTROPHY
Hypertrophy of both ventricles produces
complex electrocardiographic patterns.
Not the simple sum of the two sets of
abnormalities.
The effects of enlargement of one chamber
may cancel the effects of enlargement of the
other.
Sensitivity 20%, although the specificity was
high at 94%
65. BVH CRITERIA
LVH + Prominent R waves in right precordial
leads.
Voltage criteria for LVH + RAD
LAE as sole criterion for LVH + RVH.
ECG evidence of LVH with clockwise
rotation of heart.
Large equiphasic QRS complex in mid
precordial leads.
66. Katz-Wachtel pattern
•Katz – wachtel phenomenon: Large equiphasic QRS complex in mid
precordial leads (V2-4).
•Seen in largeVSD with biventricular enlargement
•R+S > 45 in adults, > 60 in children
67. Chamber enlargement in
pediatric age group
Related to changes in LV:RV mass.
Birth : RV is thicker than LV.
Large increase in LV weight during first month.
LV:RV reaches 2:1 by 6 months of age.
At birth 0.8:1
1 month 1.5:1
6 months 2.0:1
Adult 2.5:1
LV:RVWEIGHT RATIO
68. Normal ECG
New borns and infants < 2 month - RAD and RV dominance.
> 3 years - Resembles adult ECG.
1 month and 3 years – ECG’s are intermediate.
T waves inV1 are almost always negative.
4 week infant
69. Atrial abnormality
RAA - Peaked P wave in leads II andV1
3 mm in infants < 6 months
>2.5 mm in infants > 6 months.
LAA- Prolongation of P wave duration
12 mths->0.10 sec.
< 12 mths ->0.08 sec.
Terminal or deeply inverted P wave inV1 orV3R
Broad and notched P wave in II, biphasic inV1.
[Emerg Med Clin N Am 24 (2006) 195–208,The Pediatric ECG]
70. RVH
R wave greater than the 98th percentile in lead
V1.
S wave greater than the 98th percentile in lead I
orV6.
RSR’ pattern in leadV1,
R’ height > 15 mm in infants <1 yr or
R’ height > 10 mm in children >1 yr
UprightT-wave inV1 (>7 days, upto 10 years)
qR pattern in leadV1
Overall Sensitivity 69%, specificity 82%
71.
72. LVH
R-wave amplitude greater than 98th percentile in
leadV5 orV6.
R wave less than 5th percentile in leadV1 orV2
S-wave amplitude greater than 98th percentile in
leadV1.
Q wave greater than 4 mm in leadV5 orV6
InvertedT wave in leadV6
73.
74. Suggested reading / References
An Introduction to Electrocardiography – Leo
Schamroth 7th ed
Marriott’s Practical Electrocardiography 11th
ed
Advanced 12-lead Electrocardiography;
Cardiology Clinics August 2006
AHA/ ACCF / HRS recommendations for the
standardisation and interprertation of the
Electrocardiogram PartV. JACC 2009; 53:
992-1002
Increased duration and depth of the terminal negative portion of the P wave in lead V1 so that the area subtended exceeds 0.04 mm.sec
The QRS will be predominantly upright in leads I, II, III, aVL, aVF, V4, V5, and V6.
> Normally, a progressive increment in the amplitude of the R wave occurs from leads V1 through V6 while small q waves begin to appear from leads V4 through V6.
The R wave begins as a small (<7 mm) upright waveform in lead V1 and becomes progressively taller across the left precordia leads.
In addition, the S wave is deep in lead V1 and becomes progressively smaller across the left precordial leads
Leads I, aVL, or V6 will show a small initial q wave, representing the mean septal vector traveling away from the +ve electrode of these leads
The normal QRS duration is 0.06 to 0.10 seconds