This document describes the electrocardiographic features of atrial flutter. It discusses:
- Typical atrial flutter involves a macroreentrant circuit around the tricuspid valve that rotates either clockwise or counterclockwise.
- Atypical flutter has a less well defined circuit and rate over 350 bpm.
- ECG shows sawtooth flutter waves at 250-350 bpm without isoelectric segments. The ventricular response is typically 2:1 but can be variable.
- Counterclockwise flutter has negative flutter waves in inferior leads and positive in V1. Clockwise is reversed.
- Right versus left atrial flutter can be distinguished by the polarity of flutter waves in V1
Tachycardias are broadly categorized based upon the width of the QRS complex on the electrocardiogram (ECG). A narrow QRS complex (<120 milliseconds) reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the His bundle (ie, a supraventricular tachycardia). The site of origin may be in the sinus node, the atria, the atrioventricular (AV) node, the His bundle, or some combination of these sites. A widened QRS (≥120 milliseconds) occurs when ventricular activation is abnormally slow. The most common reason that a QRS is widened is because the arrhythmia originates below the His bundle in the bundle branches, Purkinje fibers, or ventricular myocardium (eg, ventricular tachycardia). Alternatively, a supraventricular arrhythmia can produce a widened QRS if there are either pre-existing or rate-related abnormalities within the His-Purkinje system (eg, supraventricular tachycardia with aberrancy), or if conduction occurs over an accessory pathway. Thus, wide QRS complex tachycardias may be either supraventricular or ventricular in origin.
Tachycardias are broadly categorized based upon the width of the QRS complex on the electrocardiogram (ECG). A narrow QRS complex (<120 milliseconds) reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the His bundle (ie, a supraventricular tachycardia). The site of origin may be in the sinus node, the atria, the atrioventricular (AV) node, the His bundle, or some combination of these sites. A widened QRS (≥120 milliseconds) occurs when ventricular activation is abnormally slow. The most common reason that a QRS is widened is because the arrhythmia originates below the His bundle in the bundle branches, Purkinje fibers, or ventricular myocardium (eg, ventricular tachycardia). Alternatively, a supraventricular arrhythmia can produce a widened QRS if there are either pre-existing or rate-related abnormalities within the His-Purkinje system (eg, supraventricular tachycardia with aberrancy), or if conduction occurs over an accessory pathway. Thus, wide QRS complex tachycardias may be either supraventricular or ventricular in origin.
How to follow up a patient with a pacemakerYasmeen Kamal
For the craziest medical doctors on earth who love cardiology and electrophysiology , for nuts and dreamers who try to make this world a better place ... how to follow up a patient with a pacemaker ?
themed "Her" movie
How to follow up a patient with a pacemakerYasmeen Kamal
For the craziest medical doctors on earth who love cardiology and electrophysiology , for nuts and dreamers who try to make this world a better place ... how to follow up a patient with a pacemaker ?
themed "Her" movie
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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.
Best Ayurvedic medicine for Gas and IndigestionSwastikAyurveda
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
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
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
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.
- 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
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- 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
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
2. • Atrial flutter is characterized by a rapid, regular atrial rhythm at a rate
of 250 to 350 beats/min.
• There are usually no isoelectric segments between the regular,
uniformly shaped, biphasic, sawtooth-like oscillations.
• Most commonly the ventricular response in the absence of
treatment is 2:1 but may be 4:1, 3:1, 3:2, or any other manifestation
of atrioventricular (AV) block .
3. Type I, or typical, atrial flutter
• macroreentrant atrial tachycardia.
• type I flutter requires the isthmus of tissue between the inferior vena
cava (IVC) and tricuspid annulus as a necessary component, it is often
referred to as "isthmus-dependent" flutter.
• common form (=90%) of isthmus-dependent flutter, the reentrant
circuit rotates around the tricuspid annulus in a counterclockwise
direction.
• Less often(10%), the reentrant circuit rotates in the opposite
direction, type I, typical, isthmus-dependent flutter, "reverse", or
"clockwise" flutter.
4. Type II, or atypical, atrial flutter
• was considered unclassified because the mechanisms are not fully
understood.
• any tachycardia fulfilling the classic ECG definition of a continuously
undulating pattern but not fitting the typical flutter patterns
(counterclockwise or clockwise) .
• The main distinguishing characteristics were an atrial rate greater
than 340 or 350 beats/min
• the inability to be entrained.
5. Scheinman et al classification
• CAVO-TRICUSPID ISTHMUS-DEPENDENT ATRIAL FLUTTER
• NONCAVOTRICUSPID-DEPENDENT ATRIAL FLUTTER
6. CCW Atrial Flutter
• Typical
• Most common type - 90%
• From a left anterior oblique (LAO) fluoroscopic view, the circuit
rotates in a CCW direction
7. cranial caudal activation
sequence along the right
atrial lateral wall,
across the cavotricuspid
isthmus in a lateral-to-
medial direction
superiorly in the right atrial
septum
8. Clockwise (CW) Atrial Flutter
• Reversed version of CCW AFL
• 10%
• same boundaries as its counterclockwise counterpart
9. ELECTROCARDIOGRAM IN TYPE I ATRIAL FLUTTER
• P waves are absent.
• Biphasic "sawtooth" flutter waves (F waves) are present at a rate of
about 300 beats/min, with the range for type I being 250 to 350
beats/min; in comparison, the flutter rate is 340 to 440 beats/min in
type II flutter .
• The F waves usually do not have an isoelectric interval between them,
unless the rate of the atrial flutter is slow.
• F waves have the appearance of a down sloping segment followed
by a sharp negative deflection, a sharp positive deflection that may
have a positive overshoot leading into the next downward deflection .
10. Counter-clockwise flutter
• Lead V1 -initial isoelectric component followed by an upright
component.
• With progression across the precordium, the initial component
rapidly becomes inverted and the second component isoelectric
usually by V2 to V3
• this produces the overall impression of an upright flutter wave in V1
which becomes inverted by V6.
• Lead I is low amplitude/isoelectric
• aVL usually upright.
11. clockwise flutter
• inferior leads- flutter waves are usually broadly positive, with characteristic
notching.
• However, there is an inverted component preceding the upright notched
component.
• Depending on the amplitude of this component, the appearance can be of
continuous undulation without an obviously predominant upright or inverted
component
• On other occasions, it may appear that the inverted component is dominant,
thus superficially mimicking counterclockwise flutter.
• V1 -broad negative and usually notched deflection
• transition across the precordium to an upright deflection in V6.
• Lead I -upright
• aVL - low amplitude negative and notched
16. • The ventricular response (R-R intervals) is usually one-half the rate of the atrial
input (ie, 2:1 AV nodal conduction with a ventricular response of about 150
beats/min).
• AV block greater than 2:1 in the absence of drugs that slow the ventricular
response suggests AV nodal disease which, in turn, may be part of the sick sinus
or tachy-brady syndrome.
• 1:1 AV response suggests accessory bypass tracts, sympathetic excess, and
parasympathetic withdrawal
• Even ratios of input to output (eg, 2:1, 4:1) are much more common than odd
numbers (eg, 3:1, 5:1).
• Odd ratios and shifting ratios (eg, alteration of 2:1 with 4:1) probably reflect
bilevel block in the AV node.
• The QRS complex is narrow unless there is functional aberration, preexisting
bundle branch or fascicular block, or preexcitation.
17. • The general rule is the shallow stroke (one with a lesser slope) is to
be termed as antegrade / initial deflection that will determine the
direction of flutter waves.
• In lead the polarity of F waves in V1 it will be opposite of that of
inferior leads.
18. • aVF/lead I flutter wave amplitude ratio was > 2.5 in all
counterclockwise but < 2.5 in all clockwise atrial flutters.
• The flutter wave nadirs in the inferior leads corresponded to the
upstrokes in V1 in all counterclockwise atrial flutters, but
corresponded to the downstrokes in V1 in all clockwise atrial flutters.
19.
20. • typical atrial flutter (AFL)
• negative flutter waves in leads II, III, and aVF
• positive flutter waves in lead V1
• reverse typical AFL
• positive flutter waves in inferior leads
• negative flutter waves in lead V1
21.
22.
23. ECG features of type II AFL
• P waves are absent.
• Biphasic flutter waves (F waves) are present at a rate of 340 to 440
beats/min.
• The F waves usually do not have an isoelectric interval between them.
• There often is more apparent positivity in the F waves recorded in
the inferior leads.
• The F waves are regular and have a rather constant amplitude,
duration, morphology, and reproducibility throughout the cardiac
cycles. This uniformity distinguishes type II atrial flutter from coarse
atrial fibrillation.
24.
25. Right atrial flutter
• Circuits due to anatomic obstacles that exist remote from the CTI.
• Right atrial scars due to surgical repair of congenital heart defects
serve as anatomic obstacles for macro-reentry.
• Scars in the posterolateral and inferolateral right atrium have been
found to be involved in flutter circuits.
• The ECG appearance of free wall AFL is highly variable
• Hallmark for a right atrial free wall flutter– inverted flutter wave in V1.
• Depending on the predominant direction of septal activation, right
atrial free wall flutter can mimic either clockwise or counterclockwise
flutter
26.
27. Left atrial flutter
• less common
• Association with SHD including hypertension, mitral valve disease, left
atrial dilation, and cardiac failure.
• Circuits occur around regions of spontaneous scarring frequently
located in the posterior LA.
• Circuits may propagate around the mitral valve annulus, around
regions of scarring, and the ostia of the pulmonary veins or
infrequently may involve the septum rotating around the fossa ovalis.
• Surface ECG findings are variable, though the flutter wave amplitude
tends to be low.
28. Left atrial flutter
• The flutter wave usually shows a prominent positive deflection in lead
V1 and uncommonly is flat or isoelectric.
• The flutter waves in leads II, III, and aVF may be upright but are
frequently of low amplitude
• Owing to a high prevalence of generalized atrial disease and slower
conduction, longer cycle lengths with a greater isoelectric interval
between flutter waves have been observed.
• Mimic a focal atrial tachycardia
29.
30. right-sided vs. left-sided
• A broad-based upright V1 is highly predictive of a left-sided AFL.
• V1 is deeply inverted, this is highly suggestive of a right-sided flutter.
• V1 has an initial isoelectric (or inverted) component (followed by an
upright component), this is consistent with a right AFL.
• V1 is biphasic or isoelectric, it is not helpful in predicting the chamber
of origin.
31.
32. Atrial flutter
• should be considered in all regular narrow complex tachycardia with a
ventricular rate of ~150 bpm.
• Vagal manoeuvres may help differentiate sinus tachycardia from atrial
flutter.
• In atrial flutter vagal manoeuvres may be ineffective or result in a
rapid decrease in rate allowing flutter waves to be more easily seen.
• In atrial flutter with variable block the R-R distances will be multiples
of each other unlike atrial fibrillation in which no relationship exists
e.g. assuming atrial rate of 300bpm the R-R distance in 2:1 block is
400ms, in 3:1 block 600ms, in 4:1 block 800ms.
33. NARROW QRS TACHYCARDIA
• RESPONSE
• slowing of SA nodal activity can cause a temporary decrease in
the atrial rate (in patients with sinus tachycardia).
• slowing of AV nodal conduction can lead to AV nodal block,
which may "unmask" atrial electrical activity (ie, reveal P waves
or flutter waves) by decreasing the number of QRS complexes
that obscure the electrical baseline.
• Carotid sinus massage
34. NARROW QRS TACHYCARDIA
• some narrow QRS complex tachycardias that require AV nodal
conduction (especially AVNRT and AVRT)= the transient
slowing of AV nodal conduction can terminate the arrhythmia
by interrupting the reentry circuit.
• Less commonly, CSM can cause some atrial tachycardias to
slow and terminate.
• In some cases, no response is obtained.
Carotid sinus massage
37. NARROW QRS TACHYCARDIA
• Termination of the arrhythmia
• Termination with a P wave after the last QRS complex is
• most common in AVRT or AVNRT and is rarely seen with AT.
• Termination with a QRS complex can be seen with
• AVRT, AVNRT, or AT.
• If the tachycardia continues despite successful induction of at
least some degree of AV nodal blockade, the rhythm is almost
certainly AT or atrial flutter; AVRT is excluded and AVNRT is
very unlikely
Carotid sinus massage
38. A FLUTTER vs
• Focal atrial tachycardias classically exhibit alterations in cycle length with
speeding (‘warm up’) and slowing (‘cool down’) at the onset and
termination of tachycardia.
• The tachycardia cycle length is less helpful in differentiating between focal
and macro-re-entrant mechanisms. Although the cycle length is usually
≥250 ms in focal atrial tachycardia, shorter cycle lengths are now well
described. In this situation, particularly in the presence of intra-atrial
conduction delay, there may be no observable isoelectric interval between
P-waves, and an undulating baseline resembling AFL may be seen.
• conversely, macro-re-entrant circuits may have long cycle length in the
presence of SHD and anti-arrhythmic agents. 2 Furthermore, in the
presence of significant atrial scarring, there may be a long isoelectric
interval between flutter waves, incorrectly suggesting a focal mechanism
There are three findings that distinguish this arrhythmia from type I atrial flutter: the flutter rate is faster at 375 beats/min; there is no isoelectric interval between the flutter waves; and there is more apparent positivity in leads II, III, and avF. The high degree of AV block is due to digoxin and some underlying AV nodal disease.
This slide is from a patient with a right atrial free wall flutter (no prior surgery but mapping demonstrated spontaneous free wall
scar). Cavo-tricuspid isthmus entrainment and three-dimensional electroanatomic mapping confirmed that the CTI was not part of the circuit.
The right panel shows the flutter wave morphology prior to CTI ablation, which was performed first. The flutter wave is deeply inverted in V1
(right atrium free wall) and in inferior leads because of predominant passive activation of the septum and left atrium from inferior to superior.
In the left panel, following CTI ablation there is a dramatic change in the flutter wave morphology due to change in the activation pattern of
the septum and left atrium. This example emphasizes the dependence of flutter wave morphology on propagation patterns distant to the
circuit. Prior surgery or ablation can thus markedly influence the flutter appearance.