Primary Prevention Of Sudden Cardiac Death - Role Of DevicesArindam Pande
ICD is most cost‑effective when used for patients at high‑risk of arrhythmic death and low‑risk of other causes of death.
Specific patient populations are now recognized for whom the benefit of ICD therapy outweighs any risks
Categorizing patients on the basis of only LVEF and NYHA Functional Class can aid in identification of patients who have highest benefit from primary preventions
Primary Prevention Of Sudden Cardiac Death - Role Of DevicesArindam Pande
ICD is most cost‑effective when used for patients at high‑risk of arrhythmic death and low‑risk of other causes of death.
Specific patient populations are now recognized for whom the benefit of ICD therapy outweighs any risks
Categorizing patients on the basis of only LVEF and NYHA Functional Class can aid in identification of patients who have highest benefit from primary preventions
Reverse Takotsubo Cardiomyopathy Following General AnaesthesiaPremier Publishers
Reverse takotsubo cardiomyopathy(r-TTC) is a rare condition in which regional wall motion abnormalities affect the basal segments of left ventricle in absence of significant coronary artery disease. The Diagnosis is established by characteristic echocardiographic findings, clinical manifestations, and laboratory features. In this report we demonstrate a case of general anaesthesia induced cardiomyopathy in 21 years old female.
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.
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.
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
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
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
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
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
2. Definition
Epidemiological Overview
Risk Factors
Etiologies
SIDS & SCD in Children
Clinical Features
Management
Prevention of SCD
3. SCD is a natural death from cardiac causes heralded by
abrupt loss of consciousness within 1 hr of the onset of an
acute change in cardiovascular status.
Preexisting heart disease may or may not have been known to be
present but time & mode of death are unexpected.
Key Elements– NATURAL, RAPID , UNEXPECTED
4. In the context of time, sudden is defined for most
clinical and epidemiologic purposes as 1 hour or less
between a change in clinical status heralding the
onset of the terminal clinical event and the cardiac
arrest itself.
To satisfy clinical, scientific, legal, and social
considerations, four temporal elements must be
considered: (1) prodromes, (2) onset of terminal
event, (3) cardiac arrest, and (4) biologic death
6. TERM DEFINITION MECHANISMS
Sudden
cardiac
death
Sudden, irreversible cessation of all
biologic functions
—
Cardiac
arrest
Abrupt cessation of cardiac
mechanical function, which may be
reversible by a prompt intervention
but will lead to death in its absence
Ventricular fibrillation,
ventricular tachycardia,
asystole, bradycardia,
pulseless electrical activity,
mechanical factors
Cardiovas
cular
collapse
Sudden loss of effective blood flow
due to cardiac and/or peripheral
vascular factors that may reverse
spontaneously (e.g.,
neurocardiogenic syncope; vasovagal
syncope) or require interventions
(e.g., cardiac arrest)
Same as cardiac arrest, plus
vasodepressor syncope or
other causes of transient
loss of blood flow
7. EPIDEMIOLOGY OF SCD
Approx. 5,00,000 CASES IN U.S.A PER ANNUM
In India its around 7 Lakhs per year
Accounts for 10-15% of natural deaths and 50 % deaths
from cardiac causes.
BIMODAL AGE DISTRIBUTION with peaks between
birth and 6 months of age & after 65 yrs of age
Male preponderance
May be the first presentation of cardiovascular disease
in 25% of patients
9. Prior Episode of V.TACH
Low LVEF.
Previous Myocardial Infarction.
Coronary Artery Disease
Family History of SCD.
Cardiomyopathy
Congestive Heart Failure
Long QT Syndrome.
Right Ventricular Dysplasia.
Risk Factors of Sudden Cardiac Death (SCD)
10. Emerging markers of SCD:
Microvolt T wave alternans
Contrast enhanced MR imaging of
postinfarction border
QT Variability
MIBG Imaging
Derivatives of heart rate variability methods
Familial clustering
11.
12. Three Basic ECG Patterns with
Cardiac Arrest
Ventricular tachyarrhythmia-- ventricular fibrillation
(VF)/sustained type of pulseless ventricular
tachycardia
Ventricular asystole or a brady-asystolic rhythm with
an extremely slow rate
Pulseless electrical activity (PEA), previously referred
to as electromechanical dissociation.
16. Indian study
Most of SCD
occurred in the first
year
VALIANT study
~25% of SCD
occurred in the first
month
65% occurred after
90 days
Rao B H . Global burden of Sudden Cardiac Death and insights from India. Indian heart journal 6 6 ( 2 0 1 4 ) s 1 8 es 2 3
17. CORONARY ARTERY DS HYPERTROPHIC CMP
•Previous cardiac arrest
•Syncope
•Prior AMI within 6 months
•EF < 30%
•History of frequent ventricular
ectopics
•Family H/O SCD
•Previous cardiac arrest
•Syncope
•LV Wall thickness> 30 mm
•Drop in SBP on exercise
•Repetitive NSVT on holter
•Extensive/diffuse late gadolinium
enhancement in contrast CMR
18. DCMP VAVULAR HEART DS LONG QT
SYNDROME
•Previous cardiac
arrest
•Syncope
•EF of 30-35%
•Use of inotropes
•Valve replacement
within past 6 months
•Syncope
•H/O frequent
Ventricular ectopics
•Symptoms a/w severe
uncorrected AS or MS
•Family H/O long QT &
SCD
•Medications that
prolong QT
•Bilateral deafness
19. Acquired disease of the AV node and His-Purkinje system
& the presence of accessory pathways of conduction
Risk group-
Anterior AMI with RBBB/Bifascicular block
Primary fibrosis/secondary(Lenegre/Lev)with intramural
conduction defect
Aberrant pathway with short anterograde pathway
SYNDROMIC PESENTATION-
Long-QT Syndromes
Short-QT Syndrome
Brugada Syndrome
Early Repolarization Pattern and SCD
Catecholaminergic Polymorphic Ventricular Tachycardia
Electrical Instability Resulting from Neurohumoral and Central
Nervous System Influences
20. SIDS (birth and 6 months ) had an incidence of 1.2
deaths/1000 live births
SIDS deaths related to longer QT intervals and related
arrhythmias-mutation of Na channel(SCN5A)
Beyond SIDS age group:
• Post CHD
surgery
25%
• 25-65%
• Older children(1-
21yrs)
cardiac causes of
sudden death • congenital aortic stenosis,
Eisenmenger syndrome,
pulmonary stenosis or
atresia, or HOCM
75%
22. Before Arrest
Hypotension (systolic
BP < 100 mm Hg)
Pneumonia
Renal failure
(BUN > 50 mg/dL)
Cancer
Homebound
lifestyle
During Arrest
Arrest duration
>15 min
Intubation
Hypotension
(systolic BP <
100 mm Hg)
Pneumonia
Homebound
lifestyle
After Resuscitation
Coma
Need for
pressors
Arrest duration
> 15 min
23. The response to a cardiac arrest is driven by two urgent
principles:
(1) maintenance of continuous artificial
cardiopulmonary support until return of spontaneous
circulation
(2) restoration of spontaneous circulation as quickly
as possible.
(1) initial
assessment
&
summoning
of an
emergency
response
team;
(2) basic
life
support
3) early
defibrillation
by a first
responder (if
available)
(4)
advanced
life
support;
(5) post–
cardiac
arrest
care.
long-
term
manag
ement
24. Observe for respiratory movement
Look at the skin color
Simultaneous palpation of major arteries
Once suspected/ confirmed call help for out of
hospital setting & arrange for early shifting to
hospital.
25. Chest Thump( Thump version):
One/two blows delivered to the junction of
middle & lower third of sternum from a height
of 8-10 inches.
If conscious forceful cough increases
intrathoracic pressure which increases forward
flow & finally convert VT/VF.
26. The CAB of Cardiopulmonary Resuscitation
Circulation:
30:2 with a rate of 100/m
Palm of one hand over lower half of sternum, heel of other rests
dorsum of hand
Force to depress the sternum at least 5 cm
Airway:
Tilting head backwads
Lifting chin
Heimlich maneuver
Breathing:
Mouth to mouth
Ambu bags
ET tubes
37. Amiodarone: Continuous infusion is preferred
Lidocaine: Particularly after ischemic events
Procainamide: If other fails
Propranolol/Esmolol: For polymorphic VT /VT
Storm in conjunction with Magnesium
Sulphate unresponsive to Amiodarone
Isoproterenol: For post defibrillation
bradycardia
38. Primary Cardiac Arrest in Acute Myocardial
Infarction(free of hemodynamic dysfunction):
Urgent intervention
Secondary Cardiac Arrest in Acute Myocardial
Infarction(with hemodynamic instability):
Aggressive hemodynamic, anti ischemic, anti arrhythmic
measures.
Cardiac Arrest Among in-Hospital Patients with Non
cardiac Abnormalities:
Withdrawal of offending drugs, correction of
electrolytes, acidosis & hypoxia.
39. The goals of the workup are to identify the specific causative
and triggering factors of the cardiac arrest, to clarify the
functional status of the patient's cardiovascular system, and to
establish long-term therapeutic strategies-
General Care-
CABG Patch trial revealed no mortality benefit of ICD after
revascularization & indications limited to generally accepted
indication for angioplasty or surgery
Cardiac arrest survivors a significant improvement in long-
term outcome observed who had received beta blockers.
MRFIT suggested a higher mortality rate in the special
intervention group, related to diuretic use and K+ depletion
Various pharmacologic strategies (ACEI,β-blocker etc) provide
SCD benefit in conjunction with total mortality benefit
41. A. Anti arrhythmic Drugs
B. Therapy Guided by Programmed Electrical
Stimulation
C. Surgical Intervention Strategies
D. Catheter Ablation Therapy
E. Implantable Defibrillators
42. Historically, assumption that a high frequency of ambient ventricular
arrhythmias constituted triggering mechanism for lethal arrhythmias and
suppression by anti arrhythmic drugs was protective.
Ambient arrhythmia suppression and empiric anti arrhythmic drug
therapy enjoyed a short period of popularity as a strategy for reduction
of risk among VT/VF survivors
Results of CAST demonstrated certain class I anti
arrhythmic drugs are neutral or harmful
Secondary analysis of a small number of events ,combination of
amiodarone and beta blocker in the post–MI patient provides greater
benefit from subgroup analysis of the EMIAT and CAMIAT Study
another study reinforced the benefit of beta blockers
for the specific prevention of SCD in unselected post–MI
patients.
43. The use of programmed electrical stimulation to identify
benefit on the basis of suppression of inducibility by an anti
arrhythmic drug gained popularity for evaluation of long-term
therapy among survivors of out-of-hospital cardiac arrest.
Nonetheless, most studies have demonstrated limitations
based on observations that a relatively small fraction of cardiac
arrest survivors had inducible arrhythmias.
Drug suppression of inducibility during electrophysiologic
testing as an endpoint for secondary prevention of SCD/
primary prevention in high-risk post–myocardial infarction
patients has yielded to the benefits of ICD therapy in most
subgroups
44. Intraoperative map-guided cryoablation may
be used for patients who have –
inducible, hemodynamically stable sustained
monomorphic VT during electrophysiologic
testing
and have suitable ventricular and coronary
artery anatomy amenable to catheter ablation.
It can be used as adjunctive therapy for ICD
recipients whose arrhythmia burden requires
frequent shocks.
45. Catheter ablation techniques to treat VT most
successful for the benign focal tachycardias
that originate in the right ventricle or left side
of the IVS
VT caused by bundle branch reentrant
mechanisms, ablation of the right bundle
branch to interrupt the reentrant cycle
catheter ablation techniques are not used for
the treatment of higher risk ventricular
tachyarrhythmias or for definitive therapy
49. A. LVEF ≤ 35%
Prior AMI≥ 40 days
NYHA class II- III
B. LVEF ≤ 30%
Prior AMI ≥40 days
NYHA class I
C. LVEF ≤ 40%
Prior AMI
Inducible VT/VF at EP study
NSVT
50. ICD Indications in Genetic Disorders Associated with Sudden Cardiac Death Risk
51. Can the young of SCD be the donor of
heart transplantation ?
Answer: NO
52. The vast majority of cases of SCD are due to ventricular
arrhythmias
The causes of SCD is different in different age groups
The most effective strategy for prevention of SCD is
implantable cardioverter defibrillator (ICD)
Strictly speaking, most victims of SCD can not be the donor of
heart transplantation
Editor's Notes
For gen population age 35 yrs and older,SCD risk is 0.1-0.2 % per yr and that among adolescents and adults younger than age 30 yrs is 1 per 1 lakh.
Risk for SCD increases dramatically beyond age 35 yrs.
Among pt >30 yrs of age, with advanced structural hrt ds, and markers of high risk for CA, the event rate may exceed 25% per yr.