This document discusses left ventricular hypertrophy (LVH) and right ventricular hypertrophy (RVH). It defines LVH as an increase in left ventricle mass due to increased wall thickness or cavity size. There are two types of LVH - systolic overload from conditions like hypertension which compromise the left ventricle during systole, and diastolic overload from things like valvular diseases which compromise it during diastole. The document outlines ECG criteria for diagnosing LVH including Sokolov-Lyon and Cornell voltage criteria. It also discusses RVH manifestations on ECG like right axis deviation, tall R waves in right precordial leads, and an S1S2S3 pattern.
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.
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.
ECG Lecture: Sinus arrest, sinoatrial exit block, AV block and escape rhythmsMichael-Joseph Agbayani
Simple ECG lecture about sinus arrest, sinoatrial exit block, AV block and escape rhythms. Slideshow was made with an audience of medical professionals in mind.
Wolff–Parkinson–White syndrome (WPW) is one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals traveling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supra-ventricular tachycardia referred to as an atrio-ventricular reciprocating tachycardia.
ECG Lecture: Sinus arrest, sinoatrial exit block, AV block and escape rhythmsMichael-Joseph Agbayani
Simple ECG lecture about sinus arrest, sinoatrial exit block, AV block and escape rhythms. Slideshow was made with an audience of medical professionals in mind.
Wolff–Parkinson–White syndrome (WPW) is one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals traveling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supra-ventricular tachycardia referred to as an atrio-ventricular reciprocating tachycardia.
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
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.
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 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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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.
2. OVERVIEW
LVH
Definition
Types of LVH
ECG changes in systolic overload
Criteria to diagnose LVH
ECG changes in diastolic overload
RVH
Definition
ECG changes
Clinical correlation
3. DEFINITION OF LVH
Increase in the mass of the left ventricle, which
can be secondary to an increase in wall thickness,
an increase in cavity size, or both.
5. Represents dominant
right to left QRS vector
Indirect representation
of left free wall
activation
Hypertrophy of
LV free wall
LEFT VENTRICULAR HYPERTROPHY
6. Systolic overload
aka Pressure overload
Resistance to LV systolic
outflow
LV compromise occurs in
systole
AS, HTN, HCM,
Coarctation of aorta
Diastolic overload
aka Volume overload
Overfilling of the LV in
diastole
LV compromise occurs in
diastole
PDA, VSD ( moderate to large
L R shunts), AR, MR
LEFT VENTRICULAR HYPERTROPHY
7. Abnormalities
of QRS
Abnormalities
of U wave
Left atrial
abnormality
Abnormalities
of QRS & T
wave axes
Abnormalities
of ST segment
& T wave LVH due
to
systolic
overload
10. Abnormalities
of ST segment
& T wave
T wave
Assymetrical
Shallow proximal
limb
T wave
Inverted in I aVL V5
V6
Upright in aVR V1 2
ST segment
Minimally
depressed with
slight upward
convexity in left
oriented leads
12. • Inverted in left oriented chest leads
• Not specific, more commonly
associated with diastolic overload
Abnormalities
of U wave
• Corroborative evidence
• Particularly useful in presence of LBBB
where it may be the only sign of LVH
Left atrial
abnormality
13.
14. QRS T WAVE AXIS
Early stage – no change in axis
Due to symmetric increase in bulk
Late stage- Left Axis deviation
Due to left anterior hemiblock
15. Progressive
widening of
QRS T angle
beyond the
normal 45
degree
T wave
tends to be
flat in lead I
Longstanding
hypertension
T wave is
maximally to
the right(+-
180 degree)
Wide frontal
and
horizontal
plane QRS –T
angles
16. Romhilt and Estes point score system
ECG finding Points
Increased QRS magnitude 3
ST T abnormalities 3
P wave of LA abnormality 3
Left axis deviation 2
Increased VAT 1
≥ 5points LVH
Mainly applicable for
LVH due to systolic overload
19. Total QRS voltage of all 12 conventional
ECG leads
20. CORNELL VOLTAGE CRITERIA
Sum of S wave in V3 and R wave in aVL>
28 mm in men and > 20 mm in women
Sensitivity is increased by multiplying with
QRS duration- CORNELL VOLTAGE
PRODUCT
> 2440 mm ms indicates LVH
22. Tall R waves
Relatively tall,
symmetrical
T wave
Inverted U
waves
Minimal ST
segment
elevation
Deep,
prominent,
narrow Q
waves
LVH due
to
diastolic
overload
28. Right free wall
• Tall R waves in
right precordial
leads
• Mean frontal QRS
axis to the
region of 120
Right Para septal
wall
• Tall R waves of
RS complexes in
mid precordial
leads
• 90 to 120
Right basal region
• rS complexes in
v1 to v6with
deep s waves v5
v6
• qR complexes in
aVR
• Terminal S waves
in all 3 standard
leads- SI SII SIII
syndrome
• Mean frontal QRS
is directed to the
right superior
quadrant
29.
30. Right Axis
Deviation
Dominant R
wave in right
sided leads
Initial
“incident” of
QRS in V1
Increased VAT
in V1
RS or rS
complexes in left
leads
RS complexes in
mid precordial
leads
Clockwise
rotation
RBBB
QRS
manifestations
of basal RVH
QRS
manifestations
31.
32. Right axis deviation
R in V1 > 6 mm
qR complex in V1
(R in V1) + (S in V5 or
V6) >10.5 mm
R/S ratio in V1 >1
S/R ratio in V6 >1
Increased VAT in V1
Right bundle branch
block
ST-T wave
abnormalities ("strain")
in right precordial leads
Right atrial abnormality
S1S2S3 pattern
S1Q3T3 pattern
33. • Minimally depressed
• Slight upward convexity
Abnormalities
of ST segment
• T wave inversion in right oriented leads (V1 to
V4)
• Most marked in V1 V2 & diminishes
progressively in amplitude
Abnormalities
of T wave
• Decreased in amplitude or even inverted in
right precordial leads &/or inferior leads
Abnormalities of
U wave
34. • RVH is frequently associated with
right atrial abnormality
• Manifests as a tall & peaked P wave
in standard lead II
Abnormalities
of P wave
38. BIVENTRICULAR HYPERTROPHY
Biventricular Hypertrophy
ECG OF LVH
associated with
RAD
degree of
clock wise
rotation (
particularly
seen in RVH
with RV
dilatation
Relatively
tall R wave
in V1 (R/S
>1)
When P wave of
LAA is seen with
Right Axis
deviation of
QRS to right
of 90
degree
S wave in
lead V5 or
lead V6
equal to or
greater
than 0.7
mV
R/S ratio in
lead V5 or
V6 equal to
or less than
1
39. TAKE HOME MESSAGE
DIAGNOSING LVH
SOKOLOV LYON CRITERIA
VOLTAGE IN aVL
NON VOLTAGE CRITERIA
CLINICAL CORRELATION
DIAGNOSING RVH
LVH as a consequence of hypertension usually presents with an increase in wall thickness, with or without an increase in cavity size..
R wave progression
Standard lead I-left oriented lead – qR complex similar to V6
rS in right oriented leads (V1 V2)
RS Rs in v3 v4
qR in the left oriented leads (I aVL V4 V5 V6)
What does S wave in right leads & R wave in left leads represent?
In LVH, LV is under strain, probably d/t relative LV ischemia, so T wave vector runs away towards the right… bad friend !!!!!
T wave has a relatively blunt apex or nadir
ST segment has opposite changes in right oriented leads (Minimally elevated with slight upward concavity in left oriented leads)
QRS & T wave axis in frontal & horizontal planes; In longstanding LVH, axis deviates to left bcz of fibrosis which affects the anterosuperior division of LBB l/t LAHB (initially incomplete & progressively becomes more advanced).
When LVH is complicated by AR or cardiac failure, LAD maybe even more marked; indicates an adverse prognosis
Inverted U wave: reason unknown; sensitive sign of impaired LV, but rarely sought
In early stage mean QRS vector is increased in amplitude but no change in axis ( 50 to 60 degree)
Commonly directed to the direction of 0 in the hemiaxial referrance system
When LVH of systolic overload is complicated by aortic incompetence or cardiac failure the
left axis deviation is more marked.
This is an adverse prognostic sign
Cornell voltage sensitivity is increased by multiplying with QRS; For calculating CV Product, a correction factor of mm is added to cornell voltage
Cornell Voltage Product overestimates LVH in the presence of obesity whereas Sokolow Lyon criteria underestimates it
QRS voltages are affected by many factors including age, gender, body habitus, race etc. The common criteria best apply to adults >35yrs of normal built
Sum of S wave in V1 and R wave in V5 or V6 exceeds 3.5 mV ( 35 mm with normal standardisation)
Sensitivity 22%
The common criteria is best applied for adults >35 years of age and moderate build
Correction factor of 8 mm is added for women for cornell voltage pdt
All above manifestations are in left oriented leads
RVH results in generation of increased QRS forces that directed anteriorly & to the right. (??? so positive QRS in V1 , V2 & aVR)
In basal region hypertrophy, QRS forces are directed superiorly, somewhat posteriorly & to the right
RAD: most common manifestation; if hypertrophy of basal region is involved,it goes further to the right & in extreme cases may cause NWAD
If RVH + NWAD is present, it indicates the presence of additional complicating factors like IV conduction defects like LAHB (seen in TOF, noonans syndrm)
2) Dominant R wave in right sided leads: due to combined effect of R paraseptal & R free wall vectors, but principally the RV free wall vector
3) Initial “incident” of QRS in V1: small initial slurring of QRS or rR’ deflections (in ASD) or qR complex (indicates RVH + RAA Eg: TR)
4) Increased VAT: corroborative evidence of right free wall ventricular hypertrophy, provided there is no RBBB
5) RS or rS complexes in I aVL V5 V6: rS complex in V6 is particularly indicative of RVH
6) RS complexes in mid precordial leads:
7) Clockwise electrical rotation in longitudinal axis: transition zone shifted to left (V4,V5 or V5,V6)
8) QRS manifestations of basal RVH: uncommon;
V1 V2 dominantly negative or rS complex V5 V6 deep S waves of rS complexes aVR tall R waves of qR complex
Frontal plane QRS axis may be deviated to the NW axis
there may be terminal S waves in all 3 standard leads SI SII SIII syndrome
T wave runs away from the area of mischeif.
Katz Wachtel phenomenon: VSD in newborns & infants shows tall biphasic QRS complexes in midprecordial leads (R + S >40mm)
3. R/S >1 seen in eisenmenger syndrome(VSD with PAH)