A comprehensive approach to Atrial Fibrillation. Everything you need to know about Atrial fibrillation. Including recent 2014 AHA guidelines of management.
A comprehensive approach to Atrial Fibrillation. Everything you need to know about Atrial fibrillation. Including recent 2014 AHA guidelines of management.
Tachy Arrhythmias - Approach to ManagementArun Vasireddy
Tachyarrhythmias are disorders of heart rhythm which may present with a tachycardia i.e. a heart rate >100 bpm.
This article provides an overview of tachyarrhythmias in general and goes on to cover the most common tachyarrhythmias in more detail. The acute management of tachyarrhythmias, in an emergency setting, will be covered in the 'Acute' section of the fastbleep website.
Tachyarrhythmias are clinically important as they can precipitate cardiac arrest, cardiac failure, thromboembolic disease and syncopal events. As such, they crop up time and time again in exam papers and on the wards.
Tachyarrhythmias are classified based on whether they have broad or narrow QRS complexes on the ECG. Broad is defined as >0.12s (or more than 3 small squares on the standard ECG). Narrow is equal to or less than 0.12s. Broad QRS complexes are slower ventricular depolarisations that arise from the ventricles. Narrow complexes are ventricular depolarisations initiated from above the ventricles (known as supraventricular). One important exception is when there is a supraventricular depolarisation conducted through a diseased AV node. This will produce wide QRS complexes despite the rhythm being supraventricular in origin.
LECTURE ON ATRIAL FIBRILLATION TO 9TH TERM MEDICAL STUDENTS REFERENCES: DAVIDSON(2018) HARRISON 20TH ED OF MEDICINE AND 2020 EUROPEAN HEART GUIDELINES ON AF
The following powerpoint presentation is about the current AF guidelines, prepared by Dr Jawad Siraj, who is a final year resident as Cardiology Unit, PGMI, LRH, Peshawar
Tachy Arrhythmias - Approach to ManagementArun Vasireddy
Tachyarrhythmias are disorders of heart rhythm which may present with a tachycardia i.e. a heart rate >100 bpm.
This article provides an overview of tachyarrhythmias in general and goes on to cover the most common tachyarrhythmias in more detail. The acute management of tachyarrhythmias, in an emergency setting, will be covered in the 'Acute' section of the fastbleep website.
Tachyarrhythmias are clinically important as they can precipitate cardiac arrest, cardiac failure, thromboembolic disease and syncopal events. As such, they crop up time and time again in exam papers and on the wards.
Tachyarrhythmias are classified based on whether they have broad or narrow QRS complexes on the ECG. Broad is defined as >0.12s (or more than 3 small squares on the standard ECG). Narrow is equal to or less than 0.12s. Broad QRS complexes are slower ventricular depolarisations that arise from the ventricles. Narrow complexes are ventricular depolarisations initiated from above the ventricles (known as supraventricular). One important exception is when there is a supraventricular depolarisation conducted through a diseased AV node. This will produce wide QRS complexes despite the rhythm being supraventricular in origin.
LECTURE ON ATRIAL FIBRILLATION TO 9TH TERM MEDICAL STUDENTS REFERENCES: DAVIDSON(2018) HARRISON 20TH ED OF MEDICINE AND 2020 EUROPEAN HEART GUIDELINES ON AF
The following powerpoint presentation is about the current AF guidelines, prepared by Dr Jawad Siraj, who is a final year resident as Cardiology Unit, PGMI, LRH, Peshawar
During atrial fibrillation, the heart's upper chambers — called the atria — beat chaotically and irregularly. They beat out of sync with the lower heart chambers, called the ventricles. For many people, AFib may have no symptoms. But AFib may cause a fast, pounding heartbeat, shortness of breath or light-headedness.
This presentation describes the epidemiology, initial assessment, investigation and emergency department management of a patient with atrial fibrillation. Some new research evidences are also discussed to answer some dilemmas.
Atrial Fibrillation is the most common arrhythmia encountered by a physician. The global prevalence is increasing because of aging population and better detection methods. Prediction of new onset AF is possible. AF is also a lifestyle disease. Lifestyle therapy, rate or rhythm control and stroke risk stratification are are four main pillars of AF management.
Atrial fibrillation with emphasis on managementRaghavAgrawal94
Comprehensive slides on the history, risk factors, pathophysiology, clinical features, diagnosis, management, complications and trials of Atrial Fibrillation(AF/AFib) for the use of Internal medicine residents or physicians
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.
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.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
- 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
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
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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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.
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
1. D . B A S E M E L S A I D E N A N Y
L E C T U R E R O F C A R D I O L O G Y
A I N S H A M S U N I V E R S I T Y
Atrial fibrillation
2. --Most common cardiac arrhythmia.
--Characteristics:
•The RR intervals “irregularly irregular.”
•There are no distinct P waves. Thus, even when P-P interval can be
defined, it is not regular and often less than 200 milliseconds =atrial
rate >300 beats/minute.
--The prevalence of paroxysmal AF, which is more likely to be detected
with ambulatory monitoring, is much higher
--ATRIA study in USA (1.9 million):
•The overall prevalence of AF was 1%; 70% were at least 65 years.
•The prevalence of AF ranged from 0.1% among adults less than 55
years of age to 9% in those ≥80 years of age.
•The prevalence was higher in men than women (1.1 versus 0.8 %)
--Incidence increases with age, IHD
3. RISK FACTORS AND DISEASE ASSOCIATIONS
-Hypertensive heart disease and coronary heart disease (CHD) are the
most common underlying disorders in developed countries
-In AMI, AF develops in 6-10% due to atrial ischaemia or atrial
stretching from HF
-Rheumatic heart disease is associated with a much higher incidence
of AF in developing countries
-HF
-HCM 10-28%, prognostic imp. unclear
-Congenital heart
ASD (20%, inc with age)
Ebstein's anomaly, PDA
After surgical correction of some other abnormalities, including
ventricular septal defect, tetralogy of Fallot, pulmonic stenosis, and
transposition of the great vessels
4. -10-14% documented PE
-COPD, peripartum cardiomyopathy, lupus myocarditis, and both
idiopathic and uremic pericarditis
-Possible causal relationship between obstructive sleep apnea (OSA)
and AF
-Obese individuals (BMI >30 kg/m2) are significantly more likely to
develop AF
-Metabolic syndrome
-Hyperthyroidism:
inc beta adrenergic tone, inc thyroid hormones (increased
automaticity and enhanced triggered activity of pulmonary vein
cardiomyocytes)
-Subclinical hyperthyroidism (dec TSH)
-Possible relationship between AF and hypothyroidism has been
suggested but not proven
5. Surgery
--The incidence is greatest in patients undergoing coronary artery
bypass graft (CABG) or cardiac valve surgery.
--Cardiac surgery :
30 to 40% early post CABG
37 to 50% after valve surgery
60% valve replacement plus CABG
10 to 24% of patients with a denervated transplanted heart, often in
the absence of significant rejection. Mostly within the first two weeks,
while AF developing after two weeks may be associated with an
increased risk of subsequent death
--Noncardiac surgery:
AF is less common after noncardiac compared to cardiac surgery.
Most episodes occurred within the first three days after surgery.
The risk was greatest with intrathoracic surgery (12%).
6. --Family history:
The presence of AF in a first-degree relative, particularly a
parent, has long been associated with an increase in risk
--Genetics:
-For the majority of patients, genetic susceptibility, if present, is
probably a polygenic phenomenon=combined effects of a
number of genes
-Some families have been identified in which AF inheritance
follows more typical Mendelian patterns, consistent with a
single disease-causing gene
-Mutations in SCN5A have also been identified in several other
cardiac disorders, including the long QT syndrome, the Brugada
syndrome, familial atrioventricular conduction block, and
familial sick sinus syndrome
7. --Birth weight:
A possible relationship between birth weight and the
development of AF
Incident AF increased significantly from the lowest to
the highest birth weight
--Inflammation and infection:
Inflammation, as determined by CRP, is not likely to be
causative of atrial fibrillation
--Pericardial fat is visceral adipose tissue with
inflammatory properties; both obesity and inflammation
are risk factors for AF
8. --Autonomic dysfunction:
The autonomic nervous system may be involved in the initiation
and maintenance of AF as both heightened vagal and
sympathetic tone can promote AF
--Other supraventricular tachyarrhythmias:
-Spontaneous transition between typical atrial flutter and AF
has been observed. In addition, AF is, in some patients,
associated with paroxysmal supraventricular tachycardia
(PSVT)
-Enhanced vagal tone, or atrial premature beat can cause stable
PSVT to degenerate into AF or retrograde conduction via the
accessory pathway of a premature beat, stimulating the atrial
myocardium during its vulnerable period
9. --Alchol:
AF occurs in up to 60% of binge drinkers with or without an
underlying alcoholic cardiomyopathy ="the holiday heart
syndrome.“ in most cases
--Caffeine:
Despite the theoretical relationship between caffeine and
arrhythmogenesis, there is no evidence in humans that
ingestion of caffeine in doses typically consumed can provoke
AF or any other spontaneous arrhythmia
--With regard to dietary fish intake and incident AF, three
cohort studies (approximately 45,000, 48,000, and 5000
individuals) found no relationship, while one (approximately
5000 individuals) suggested a reduction in AF burden
10. --Medications:
Certain medications can cause or contribute to the
development of AF =theophylline, adenosine (with the
WPW, due to conduction down the accessory
pathway), drugs that enhance vagal tone, such as
digitalis
11. Longterm outcome
1. Death : Death rate doubled (Only antithrombotic therapy has been
shown to reduce AF-related deaths).
2. Stroke (includes haemorrhagic stroke and cerebral bleeds):
Stroke risk increased; AF is associated with more severe stroke.
3. Hospitalizations:
Hospitalizations are frequent in AF patients and may contribute to
reduced quality of life.
4. Quality of life and exercise capacity:
Wide variation, from no effect to major reduction.
AF can cause marked distress through palpitations and other AF-
related symptoms.
5. Left ventricular function:
Wide variation, from no change to tachycardiomyopathy with acute
heart failure.
12. PATHOGENESIS
--Sustained AF seems to require the development of multiple wavelets
(rather than the single wavefront as seen in atrial flutter).
--Majority of episodes of paroxysmal AF (PAF) are triggered by atrial
premature beats, while a small number are preceded by typical atrial
flutter or atrial tachycardia
--Atrial premature beats appear to be most important as a trigger in
patients with PAF who have normal or near-normal hearts, much less
clear in patients with significant structural heart disease
--Ectopic foci are most often located near the pulmonary veins, in
patients with minimal or no structural heart disease
--Ablation of sites with a high dominant frequency, mostly located at
or close to the junction between the PVs and the left atrium, results in
progressive prolongation of the AF cycle length and conversion to
sinus rhythm in patients with paroxysmal AF, while in persistent AF,
sites with a high dominant frequency are spread throughout the entire
atria, and ablation or conversion to sinus rhythm is more difficult
13. --Other factors that may contribute to AF in near normal
patients include increased vagal tone and possible
subclinical myocarditis
--As AF becomes established, the refractory period of the
atrial muscle shortens (down-regulation of the L-type Ca2+
inward current, up-regulation of inward rectifier K+
currents) predisposes to further AF (ie, AF begets AF).
--Conversely, when sinus rhythm is sustained, these
electrophysiologic changes reverse (sinus rhythm begets
sinus rhythm).
--Echocardiographic risk factors: Left atrial enlargement,
increased left ventricular wall thickness and reduced left
ventricular fractional shortening.
14. Structural abnormalities associated with AF
Extracellular matrix alterations
Interstitial and replacement fibrosis
Inflammatory changes
Amyloid deposit
Myocyte alterations
Apoptosis
Necrosis
Hypertrophy
Dedifferentiation
Gap junction redistribution
Intracellular substrate accumulation (haemocromatosis, glycogen)
Microvascular changes
Endocardial remodelling (endomyocardial fibrosis)
15. Clinical correlates
1-Thrombo-embolism:
-LAA is the dominant source of embolism(90%) in non-valvular AF.
-‘Flow abnormalities’:
stasis within the left atrium,
reduced (LAA) flow velocities
spontaneous echo-contrast on(TOE).
-‘Endocardial abnormalities’:
Progressive atrial dilatation
endocardial denudation
oedematous/fibroelastic infiltration of the extracellular matrix.
-‘Abnormalities of blood constituents’:
haemostatic and platelet activation
Inflammation and growth factor abnormalities
16. 2-Haemodynamic changes:
Loss of coordinated atrial contraction (5-15% of COP)
High ventricular rates (dec filling as dec diastole)
Irregularity of the ventricular response
Decrease in myocardial blood flow
Long-term alterations such as atrial and ventricular
cardiomyopathy.
17. CLASSIFICATION (ACC/AHA/ESC)
applies to recurrent episodes of AF that last more than 30 seconds and that are unrelated to a reversible
cause
•First detected or diagnosed, irrespective of the duration or the presence or
absence of symptoms.
•Paroxysmal (ie, self-terminating or intermittent) AF:
Defined as recurrent AF (≥2 episodes) that terminate spontaneously in less
than seven days, usually less than 24 hours.
Progression to persistent and permanent AF occur in >50% beyond 10 years
despite antiarrhythmic therapy.
•Persistent AF:
Fails to self-terminate within seven days. Episodes often require
pharmacologic or electrical cardioversion to restore sinus rhythm.
The ESC recognizes a category called “long-standing persistent AF,” which
refers to AF that has lasted for one year or more when it has been decided to
adopt a rhythm control strategy.
•Permanent AF:
More than one year and cardioversion either has not been attempted or has
failed.
18. LONE AF
-Individuals with paroxysmal, persistent, or
permanent AF who have no structural heart disease.
-Less than 15 to 30% of cases of permanent AF and 25
to 45% of cases of paroxysmal AF
-Younger than those with structural heart disease and
are often male
-Often symptomatic and associate certain triggers with
episodes of AF: sleeping, exercise, alcohol, eating
-Family history of AF is present in up to 38%
19. RECURRENT AF
Continuous monitoring studies have shown that
approximately 90% of patients have recurrent episodes
of AF. However, up to 90% of episodes are not
recognized by the patient
20.
21. History and physical examination
--Not all patients with AF are symptomatic.
--Description of the symptoms: onset or date of discovery,
the frequency and duration, severity, and qualitative
characteristics.
--Typical symptoms:
palpitations, tachycardia, fatigue, weakness, dizziness,
lightheadedness, reduced exercise capacity, increased
urination, or mild dyspnea.
More severe symptoms include dyspnea at rest, angina,
presyncope, or infrequently, syncope.
some patients present with an embolic event
22. --Precipitating causes: exercise, emotion, or alcohol.
--Disease associations:
cardiovascular or cerebrovascular disease, diabetes,
hypertension, chronic obstructive pulmonary disease,
or potentially reversible causes (eg, hyperthyroidism,
excessive alcohol ingestion).
--Examination: Abnormal findings may inform about
either contributing factors for (eg, murmur of mitral
stenosis) or the impact of (eg, evidence of heart failure)
AF or complications (eg, CVS)
23. Electrocardiogram
Essential………….
--The ECG should also be evaluated for the following
information:
•Markers of nonelectrical cardiac disease, such as left
ventricular hypertrophy (possible hypertension) or Q
waves (possible coronary artery disease)
•Markers of electrical heart disease, such as delta wave or
short PR interval (preexcitation) or bundle branch block
(conduction system disease)
•The QT interval (to identify the potential risk of
antiarrhythmic therapy).
24. Echocardiogram
--To evaluate the size of the right and left atria and the
size and function of the right and left ventricles
--To detect possible valvular heart disease, left
ventricular hypertrophy, and pericardial disease
--To assess peak right ventricular pressure.
--Transesophageal echocardiography is much more
sensitive for identifying thrombi in the left atrium or
left atrial appendage.
25. Additional testing
--Exercise testing :
-For patients with signs or symptoms of ischemic heart disease
(which is not a common cause of AF).
-Help guide pharmacotherapy for AF as some antiarrhythmic
medications are contraindicated in patients with coronary artery
disease
--Holter monitoring:
-To identify the arrhythmia if it is intermittent and not captured
on routine electrocardiography
-To assess overall ventricular response rates, especially in
individuals where a rate control strategy has been chosen
--TSH should be obtained in all patients with AF
--Complete blood count, a serum creatinine, an analysis for
proteinuria, and a test for diabetes mellitus
26. EHRA score (for symptoms severity)
Classification of AF-related symptoms:
EHRA I ‘No symptoms’
EHRA II ‘Mild symptoms’; normal daily activity not
affected
EHRA III ‘Severe symptoms’; normal daily activity
affected
EHRA IV‘Disabling symptoms’; normal daily activity
discontinued