The long QT syndrome (LQTS) is a rare inherited heart condition in which delayed repolarization of the heart following a heartbeat increases the risk of episodes of torsades de pointes (TDP, a form of irregular heartbeat that originates from the ventricles). These episodes may lead to palpitations, fainting and sudden death due to ventricular fibrillation. Episodes may be provoked by various stimuli, depending on the subtype of the condition.The condition is so named because of the appearances of the electrocardiogram (ECG/EKG), on which there is prolongation of the QT interval. In some individuals the QT prolongation occurs only after the administration of certain medications.
This presentation is a simplified version of the various types of cardiac arrythmias seen in pediatric age groups. We have discussed supraventricular tachycarsias and prolonged QT syndrome in details here. Hope everyone finds it useful.
Presentation on basic principles of pediatric ecg with important examples: BY Dr. Nivedita Mishra (PGY2 PEDIATRICS, TRIBHUVAN UNIVERSITY TEACHING HOSPITAL,KATHMANDU,NEPAL)
The long QT syndrome (LQTS) is a rare inherited heart condition in which delayed repolarization of the heart following a heartbeat increases the risk of episodes of torsades de pointes (TDP, a form of irregular heartbeat that originates from the ventricles). These episodes may lead to palpitations, fainting and sudden death due to ventricular fibrillation. Episodes may be provoked by various stimuli, depending on the subtype of the condition.The condition is so named because of the appearances of the electrocardiogram (ECG/EKG), on which there is prolongation of the QT interval. In some individuals the QT prolongation occurs only after the administration of certain medications.
This presentation is a simplified version of the various types of cardiac arrythmias seen in pediatric age groups. We have discussed supraventricular tachycarsias and prolonged QT syndrome in details here. Hope everyone finds it useful.
Presentation on basic principles of pediatric ecg with important examples: BY Dr. Nivedita Mishra (PGY2 PEDIATRICS, TRIBHUVAN UNIVERSITY TEACHING HOSPITAL,KATHMANDU,NEPAL)
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
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.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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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
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- Prix Galien International Awards Ceremony
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.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
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2. OVERVIEW
1. READING OF AN ECG
2. INTERPRETATION OF ABNORMAL
FINDINGS
3. NORMAL VARIATIONS IN PEDIATRICS
4. HEART BLOCKS
5. CHAMBER ENLARGEMENTS
6. CONGENITAL HEART DISEASE
7. ARRHYTHMIAS IN CHILDREN
8. DYSELECTROLYTEMIAS
9. SOME EXAMPLES OF ECG READING
8. P waves
• Normal findings
• Upright in I, II, aVL
• Inverted in aVR
• amplitude < 2.5 mm [> 3mm abnormal]
• Duration < 9o msec [ > 120 msec abnormal]
• 1st half by RA Depolarisation & 2nd half by LA
9. ABNORMALITIES OF P WAVE
• INVERTED IN I, aVL
DEXTROCARDIA
REVERSAL OF ARM LEADS
LOW ATRIAL ECTOPICS
• FLAT P WAVE
HYPERKALEMIA
• ABSENT P WAVE
AF
AV BLOCK
PAROXYSMAL AT
10. • P- MITRALE- BROAD & NOTCHED P WAVES
MS
LARGE VSD
• P- PULMONALE- TALL & PEAKED P WAVES
TRICUSPID ATRESIA
EBSTEIN ANOMALY
TOF
Severe PS
HYPOPLASTIC RIGHT HEART SYNDROME
COMPLEX CHD
11. PR Interval
• Beginning of P wave to beginning of QRS
complex
• Normal: 120 – 200 msec
• LOWER LIMIT OF NORMAL PR
▫ <3 YR : 80 msec
▫ 3-16YR : 100 msec
▫ ADULTS : 120 msec
13. Q Wave
• By depolarisation of ventricular septum
• II, II, aVF
• Normal- 0.02 sec
• Never > 25% of R- wave
DEEP & WIDE Q WAVE
ALCAPA
MI
Q WAVE IN V1
Severe LVH
C- TGA
Single ventricle
15. QRS DURATION
AGE TIME (mSec)
PREMATURE 40
TERM INFANT 50
1- 3 YEAR 60
ADULTS 80
WIDE QRS
•RBBB
•LBBB
•WPW
•Arrythmias of ventricular
origin
16. QRS amplitude
• High voltage
▫ Ventricular hypertrophy
▫ Ventricular conduction disturbances
• Low voltage
▫ Myocarditis
▫ Pericardial effusion
17. QRS axis
• At birthRAD normal
• Causes Of LAD at birth
▫ Tricuspid atresia
▫ AV septal defects
▫ Very premature < 28 weeks
18. QT INTERVAL
• Onset of Q wave to End of T wave
• BAZETT’S FORMULA
▫ Corrected QT QTc= QT/RR
▫ Normal QTc= 0.42- 0.43 sec
▫ QTc Upto 0.49 sec is normal in 1st 6 months of life
PROLONGED QT SHORT QT
▫ Hypocalcemia - Hypercalcemia
▫ Rheumatic carditis -Digitalis effect
▫ Long QT syndromes
▫ Cardiomyopathies
▫ Head injury
▫ Severe malnutriotion
▫ Drugs
20. ST Segment
• ST elevation upto 1 mm is
normal
• ST Elevation
▫ Hyperkalemia
▫ IC Bleed
▫ Pneumothorax
▫ ALCAPA
▫ KD related Coronary artery
disease
▫ Brugada syndrome( ST +
RBBB)
• ST Depression
▫ Pressure overload strain
21. T Waves
• Look in V1
• At birth- upright
• After 7 days- inverts
• Inverted T-wave upto 7 yr
22. • UPRIGHT T WAVE IN V1 B/W 7 DAY- 7 YR
▫ RVH
• T INVERSION
▫ ALCAPA
▫ KD+ CORONARY ARTERITIS
▫ PRESSURE OVERLOAD STRAIN
• TALL TENTED T WAVE
▫ HYPERKALEMIA
▫ LVH
• FLAT T WAVE
▫ HYPOKALEMIA
▫ NEONATAL HYPOTHYROIDISM
▫ PERICARDITIS
▫ MYOCARDITIS
▫ MI
25. P WAVE IN ATRIAL HYPERTROPHY
RA ENLARGEMENT:
•Tall & peaked P
•P pulmonale
•Amplitude high > 3 mm
•Duration normal
LA ENLARGEMENT
•P mitrale
•Increased terminal negative
deflection-Diphasic P wave
•Prolonged p wave duration
29. VENTRICULAR HYPERTROPHY
GENERAL CHANGES:
• QRS Axis directed towards hypertrophied
ventricle
• QRS Amplitude increases in the direction of
ventricle hypertrophied
• change in R/S ratio: increased R/S in right
precordial leads suggest RVH and in left
precordial leads suggest LVH
• Changes in T-axis: strain pattern- wide QRS-T
angle with the T-axis outside the normal range
30. • RAD
• Tall R in V1
• Deep S in V6
• High R/S ratio in V1
• R/S ratio in V6 < 1
• Upright T in V1 b/w 7 days – 7 years
• Q wave in V1( qR or qRs pattern
• RVH+ wide QRS-T angle with T axis outside
normal range
• Persistent pattern of RV dominance
Criteria FOR RVH
31. • LAD
• Tall R in I, II, II, aVL,aVF, V5,
V6
• Deep S in V1/ V2
• R/S ratio in V1 < 1
• Deep Q wave [Q > 5 mm] +
tall symmetrical T wave in V5
& V6 (“LV diastolic load”)
• Strain pattern
• Inverted T wave in I, aVF
Criteria FOR LVH
32. • RVH + LVH in the absence of BBB /
preexcitation
• Large equiphasic QRS complexes in two or more
of the limb leads and in the mid- precordial
leads[V2-V5] KATZ-WACHTEL
PHENOMENON
Criteria FOR BVH
53. CONDUCTION ABNORMALITIES
• Bundle branch blocks are diagnosed as they
would be in adults; RBBB occurs most
commonly after repair of congenital heard
defects and LBBB is very rare
• First degree AV block and Mobitz type 1
(Wenckebach) can be a normal variant in 10% of
kids
• Complete AV block is usually congenital or
secondary to surgery
54. Sinus Bradycardia
• Deviation from NSR
- Rate < 60 bpm
▫ Etiology: SA node is depolarizing slower than
normal, impulse is conducted normally (i.e.
normal PR and QRS interval).
▫ Hypothermia, sleep, raised ICT, hypoxia, vagal
stimulation, hypothyroidism
56. 1st Degree AV Block
• Etiology: Prolonged conduction delay in the AV
node or Bundle of His.
• PR interval > 5 small divisions, 200 msec
• Causes: myocarditis, acute rheumatic fever,
drugs
57. 2nd Degree AV Block, Type I
• Deviation from NSR
▫ PR interval progressively lengthens,
then the impulse is completely blocked
(P wave not followed by QRS).
▫ Wenckebach phenomenon
58. 2nd Degree AV Block, Type II
• Deviation from NSR
▫ Occasional P waves are completely
blocked (P wave not followed by QRS).
▫ Etiology: Conduction is all or nothing (no
prolongation of PR interval); typically block
occurs in the Bundle of His.
• MOBITZ TYPE 2
59. • There’s full AV dissociation
• P waves and QRS have no definite association in
it
3rd Degree AV Block
60. RIGHT BUNDLE BRANCH BLOCK
1. Wide QRS > 120 msec ( >3 small divisions)
2. R > r in rSR
3. VAT is > 80 msec
4. ST depression
5. T inversion
• M morphology in V1
V1
“Rabbit Ears”
61. LEFT BUNDLE BRANCH BLOCK
1. Wide QRS > 120 msec ( > 3 small divisions)
2. VAT 80 msec
3. M morphology in V 6 (monophasic tall R )
4. Q wave absent in V5-V6
5. ST depression
6. T inversion
• morphology in V 6 and W in V1
70. • Due to premature conduction of atrial impulses
to ventricle via accessory pathway
• CAUSES OF WPW
1. Ebstein’s anomaly
2. c-TGA
3. HCM
4. Rhabdomyoma
WPW SYNDROME
71. •WPW- 3 features
1. Short PR interval
2. Delta wave on upstroke of
QRS
3. Slightly wide QRS> 110
msec( fusion complex)
