Arrhythmias are caused by abnormal electrical activity in the heart and can be due to improper impulse generation or conduction. They are treated using antiarrhythmic drugs that work by sodium or calcium channel blockade, prolonging the refractory period, or blocking sympathetic effects. Common antiarrhythmic drug classes include Class I membrane stabilizers, Class II drugs that decrease catecholamine effects, Class III potassium channel blockers, and Class IV calcium channel blockers. Effective treatment depends on the underlying arrhythmia and may involve drugs, cardioversion, ablation, or pacing.
What are anti-coagulants?
What are the difference between antiplatelet, anticoagulants and thrombolytics?
Coagulation cascade
Virchows Triad
Classification of anti-coagulants?
Indications of anti-coagulants?
Mechanism and site of action of different anti-coagulants?
Beta Blockers in current cardiovascular practice Praveen Nagula
betablockers are the drug of choice for prevention of progression of heart failure with mortality benefit, after the evolution of neurohormonal regulation as pathogenesis of heart failure
What are anti-coagulants?
What are the difference between antiplatelet, anticoagulants and thrombolytics?
Coagulation cascade
Virchows Triad
Classification of anti-coagulants?
Indications of anti-coagulants?
Mechanism and site of action of different anti-coagulants?
Beta Blockers in current cardiovascular practice Praveen Nagula
betablockers are the drug of choice for prevention of progression of heart failure with mortality benefit, after the evolution of neurohormonal regulation as pathogenesis of heart failure
Critical Care Summit Egypt 2015 Common Arrhythmias in the ICUDr.Mahmoud Abbas
Lecture presented by Dr Khaled Farouk at Egyptian Critical Care Summit 2015, the leading ICU event and medical exhibition in Egypt. www.criticalcareegypt.com
A Practical Approach to Ionotropes and vasopressors Aneesh Bhandary
Vasopressors are a powerful class of drugs that induce vasoconstriction and Inotropes increase cardiac contractility. Choice of an agent should be based upon the suspected underlying etiology of shock.
This presentation deals with the practical issues and controversies surrounding the use of these agents
Critical Care Summit Egypt 2015 Common Arrhythmias in the ICUDr.Mahmoud Abbas
Lecture presented by Dr Khaled Farouk at Egyptian Critical Care Summit 2015, the leading ICU event and medical exhibition in Egypt. www.criticalcareegypt.com
A Practical Approach to Ionotropes and vasopressors Aneesh Bhandary
Vasopressors are a powerful class of drugs that induce vasoconstriction and Inotropes increase cardiac contractility. Choice of an agent should be based upon the suspected underlying etiology of shock.
This presentation deals with the practical issues and controversies surrounding the use of these agents
Introduction to afib, Epidemiology of afib, etiology of afib, Clinical presentation of people with afib, Investigation and management
AF related outcomes and complications and differential Diagnosis
Journal club covid vaccine neurological complications ZIKRULLAH MALLICK
the risks of adverse neurological events following SARS-CoV-2 infection are much greater than those associated with vaccinations, highlighting the benefits of ongoing vaccination programs.
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.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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.
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
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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
2. Arrhythmia
• Arrhythmia is a term for any of a large
and heterogeneous group of conditions
in which there is abnormal electrical
activity in the heart.
2
3. Arrhythmias may be due to:
improper impulse generation
impulse conduction.
These manifest as abnormalities of:
rate or
regularity or
as disturbances in the normal sequence of
activation of atria and ventricles.
3
4. Causes of arrhythmias
A. Altered automaticity:
1. Sinus node(sinus tachy or brady)
2. ↑ vagal activity
3. ↑ sympathetic activity
4. Ectopic foci
5. Triggered Automaticity
4
5. B. Abnormal impulse conduction
• Heart blocks may produce bradyarrhythmias.
• Reentry circus conduction may produce
tachyarrhythmias.
5
7. • Altered autonomic nervous system activity
(↑ Symp activity predisposes to ventricular
dysrhythmias as VT / VF
• Drugs (beta blockers , Clonidine and other
sympatholytics, narcotics, adenosine,
antiarrythmics class I and III )
7
8. Treatment
• In many patients, the correction of
identifiable precipitating events is not
sufficient to suppress cardiac ectopic
dysrhythmias, and therefore specific cardiac
antidysrhythmic drugs may be administered.
8
9. DYSRHYTHMIAS REQUIRE TREATMENT
• 1. Persists despite removing the
precipitating cause
• 2. Hemodynamic function is compromised
• 3. Predisposes to more serious cardiac
dysrhythmias
9
10. Therapeutic effects are achieved by:
1. sodium- or calcium-channel blockade
2. prolongation of effective refractory
period
3. blockade of sympathetic effects on
the heart.
10
12. Class I - membrane stabilizers
• depress depolarization of cardiac cell
membrane
• by restricting entry of fast sodium current
resulting in reduction in the maximum rate of
rise of phase 0 of the action potential.
• This leads to slower rate of conduction,
increased threshold for excitation and
prolongation of the effective refractory period.
12
13. Ia
• lengthen action potential
• slow rate of rise of phase 0
• prolong repolarization
• prolong refractoriness by blocking potassium
channel
• prolong PR, QRS, QT
• moderate-marked sodium channel blockade
• eg quinidine, procainamide, disopyramide
13
15. Ic
• no effect on length of action potential
• markedly reduces rate of rise of phase 0
• markedly prolongs PR and QRS complex
• marked Na channel blockade
• prolong refractoriness by blocking potassium
channels
• eg flecainide
15
16. Class II
• decrease potential for arrhythmias to
develop in response to catecholamines
• eg bretylium: blocks release of sympathetic
transmitters
• beta blockers: competitive antagonists and
also block possible arrhythmogenic effect of
cAMP.
16
17. Class III
• - K channel blockers: prolong duration of
action potential with resulting prolongation of
effective refractory period
• - eg amiodarone, sotalol, disopyramide,
bretylium
17
18. Class IV
• calcium channel blockers
• slow SAN pacemaker cells and AVN
conduction by direct blockade of Ca channels
• have inportant effects on upper and middle
parts of the AV node
• may have particular value in blocing one limb
of a re-entry circuit
18
19. Site of action
• SAN, atrium
- Ia eg quinidine, disopyramide
- II beta blockers
- III eg amiodarone
- IV ? verapamil
- ? digoxin
19
26. EFFICACY AND RESULTS
• Suppression of ventricular ectopy using a
cardiac antiarrhythmic drug does not prevent
future life-threatening arrhythmias and may
increase mortality
• Survivors of cardiac arrest have a high risk of
subsequent ventricular fibrillation, and the
treatment of these patients with amiodarone
results in fewer life-threatening cardiac
events.
26
27. DECISION TO TREAT CARDIAC
DYSRHYTHMIAS
• The benefit of antiarrhythmic drugs is clearest
when it results in the immediate termination
of a sustained tachycardia
• β-adrenergic antagonists decrease mortality
after an acute myocardial infarction
27
29. Lidocaine
• Lidocaine is used principally for the suppression
of ventricular dysrhythmias (premature
ventricular contractions, ventricular tachycardia),
having minimal effects on supraventricular
tachydysrhythmias
• The efficacy of prophylactic lidocaine therapy for
preventing ventricular fibrillation after acute
myocardial infarction has not been documented,
and its use is no longer recommended.
29
30. • In adult patients with normal cardiac output,
hepatic function, and hepatic blood flow, an
initial intravenous administration of lidocaine,
2 mg/kg, followed by a continuous infusion of
1 to 4 mg/min should provide therapeutic
plasma lidocaine concentrations of 1 to 5
µg/mL.
30
31. Mechanism of Action
• delays the rate of spontaneous phase 4
depolarization by preventing or diminishing
the gradual decrease in potassium ion
permeability.
31
32. • Lidocaine is essentially devoid of effects on the
ECG or cardiovascular system when the plasma
concentration remains <5 µg/mL .
• Hypotension
• Bradycardia
• sizzures
• Its metabolites may possess cardiac
antiarrhythmic activity.
• CNS depression, apnea, cardiac arrest
32
33. Amiodarone
• potent antiarhythmic, antiadrenergic effect
• activity against refractory supraventricular and
ventricular tachydysrhythmias.
• In the presence of VT or VF that is resistant to
electrical defibrillation, amiodarone (300
mgIV) is recommended.
33
34. • Administered over 2 to 5 minutes, a dose of 5
mg/kg IV produces a prompt antidysrhythmic
effect that lasts up to 4 hours.
• prolonged elimination half-time of this drug.
• After discontinuation of chronic oral therapy,
the pharmacologic effect of amiodarone lasts
for a prolonged period (up to 60 days)
34
35. • It prolongs the effective refractory period of
all cardiac tissues, including the sinoatrial
node, atrium, atrioventricular node, His-
Purkinje system, and ventricle.
• minor negative inotropic effect.
35
36. Propanolol and esmolol
• β-Adrenergic antagonists are effective for the
treatment of cardiac dysrhythmias related to
enhanced activity of the sympathetic nervous
system
• perioperative stress, thyrotoxicosis,
pheochromocytoma
36
37. • controlling the rate of ventricular response in
patients with atrial fibrillation and atrial
flutter.
• The usual oral dose of propranolol for the
chronic suppression of ventricular
dysrhythmias is 10 to 80 mg every 6 to 8
hours.
37
39. VERAPAMIL AND DILTIAZEM
• Intravenous verapamil is highly effective in
terminating PSVT.
• 75 to 150 µg/kg over 1 to 3 minutes, followed
by a continuous infusion of about 5 µg/kg per
minute to maintain a sustained effect.
39
40. DOFETILIDE and IBUTILIDE
• are effective for the conversion of recent
onset atrial fibrillation or atrial flutter to
normal sinus rhythm.
40
41. • MEXILETINE and TOCAINIDE
orally effective amine analog of lidocaine that is
used for the chronic suppression of ventricular
cardiac tachydysrhythmias.
41
42. ADENOSINE
• slows the conduction of cardiac impulses
through the atrioventricular node.
• treatment of PSVT and WPW syndrome
• The usual dose of adenosine is 6 mgIV
followed, if necessary, by a repeat injection of
6 to 12 mgIV about 3 minutes later.
42
44. DIGOXIN
• Digitalis preparations, such as digoxin, are
effective cardiac antidysrhythmics for the
stabilization of atrial electrical activity and the
treatment and prevention of atrial
tachydysrhythmias.
44
45. • Digoxin toxicity can produce increased
ventricular ectopy and, when coupled with
bradyarrhythmias caused by digoxin toxicity,
may predispose to sustained polymorphic
ventricular arrhythmias and VF
45
46. • Drugs administered for the chronic
suppression of cardiac dysrhythmias pose little
threat to the uneventful course of anesthesia
and should be continued up to the time of
anesthesia induction.
• The majority of cardiac dysrhythmias that
occur during anesthesia do not require
therapy
46
47. • For these reasons, the pharmacologic
treatment of cardiac arrhythmias is principally
used to treat atrial fibrillation and atrial flutter
that is not responsive to catheter ablation
treatment and for patients with implantable
cardioverter-defibrillator devices who are
receiving frequent but needed electrical
shocks.
47
48. VT/VF
• Sustained polymorphic VT, ventricular flutter,
and VF all lead to immediate hemodynamic
collapse.
• Emergency asynchronous defibrillation is
therefore required, with at least 200-J
monophasic or 100-J biphasic shock.
48
49. • If the arrhythmia persists, repeated shocks
with the maximum energy output of the
defibrillator are essential to optimize the
chance of successful resuscitation.
• Intravenous lidocaine and/or amiodarone
should be administered but should not delay
repeated attempts at defibrillation.
49
50. Catheter and Surgical Ablative Therapy
• Ablation therapy is currently considered an
alternative to additional pharmacologic
therapy trials in patients with recurrent
symptomatic AF or AF associated with poor
rate control who have failed an initial attempt
at rhythm control with pharmacologic
management.
50
51. Bradyarrythmias
• Pacing in SA nodal disease is indicated
to alleviate symptoms of bradycardia.
• Surgical implantation of electrical leads
attached to a pulse generator.
• Pulse generator can sense electrical
activity generated by the heart and only
deliver electrical impulses when
needed.
51