1. Atrial fibrillation (AF) is a common arrhythmia where abnormal electrical signals in the atria cause an irregular heartbeat.
2. AF increases the risk of stroke by 5 times and is associated with increased mortality, hospitalization, and decreased quality of life.
3. Management involves rate or rhythm control as well as anticoagulation to prevent stroke, with treatment depending on factors like symptoms, age, and stroke risk level.
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LECTURE ON ATRIAL FIBRILLATION TO 9TH TERM MEDICAL STUDENTS REFERENCES: DAVIDSON(2018) HARRISON 20TH ED OF MEDICINE AND 2020 EUROPEAN HEART GUIDELINES ON AF
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 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.
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.
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
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1. ATRIAL FIBRILLATION
Dr SYED RAZA
MD,MRCP(UK),CCT(UK),MESC,Dip.Card(UK),FCCP
Consultant Cardiologist
2.
3. OBJECTIVES
• Introduction
• Classification
• Burden of the problem
• Diagnosis
• Management
4. What is it ?
• Abnormal electrical wavelets originate from
left atrium
• Propagating in different directions
• Disorganized atrial depolarisation without
effective atrial contraction
8. ECG Diagnosis
• On ECG p waves are absent and RR interval is
variable.
• f waves 350-600 beats /min.
• ventricular response is grossly irregular at
100-160 beats /min.
• Rate : No. of R waves x 10 ( 6 sec strip)
9.
10.
11. Prevalance
• 2.2 Million people in the US
• 6.5 cases/1000 examinations
• 4% > 60yrs
• 8 % > 80 yrs
• 25% of individuals aged 40 yrs and older will
develop AF in their life time.
12. Prevalence of AF in the Renfrew-
Paisley study
Cohort of men and women aged 45–64 years (n = 15,406)
Reproduced with permission of the BMJ Publishing Group from Stewart S et al, Heart 2001: 86:516-21
13. Clinical events (outcomes) affected by
AF
Outcome Parameter Relative change in AF
patients
1.Death 1.Death rate is doubled
2.Stroke 2.Stroke risk increases 5
times
3.Hospitalisation 3.More frequent
4.Quality of life and 4.Can be markedly
exercise capacity decreased
5.LV function 5.Tachycardiomyopathy/
heart failure
14. Classification of AF
Terminology Clinical features
Initial event (first Symptomatic Rhythm/Rate
detected episode) Asymptomatic
Onset unknown
Paroxysmal Spontaneous termination Rhythm
<7 days and most often Control
<48 hours
Persistent Not self-terminating Rhythm or
Lasting >7 days or prior Rate control
cardioversion
Permanent Not terminated Rate Control
(‘accepted’) Terminated but relapsed
No
cardioversion attempt
15.
16. Etiologies of AF
CARDIAC
Hypertensive heart disease
Valvular heart disease
Ischaemic heart disease
Cardiomyopathy
Pericarditis
Congenital heart disease
Post Cardiac surgery
17. Etiologies of AF contd:
NON CARDIAC
1. Pulmonary : Pneumonia, COPD,PE
2. Hyperthyroidism
3. Excess catecholamine /sympathetic activity
4. Drugs and alcohol
5. Significant electrolyte imbalance
18. LONE ATRIAL FIBRILLATION
• Younger patients < 60
• No underlying cause
• Usually not much symptoms
• Normal heart structure
• No associated co-morbidities
19. Why AF management is
important?
• extremely common
• Can lead to symptoms
• potentially serious consequences:
– embolism
– impaired cardiac output
– increased mortality
20. Management of Acute AF (<48 hrs)
• Haemodynamically unstable :
hypotension/heart failure/chest pain/syncope
Use DC Cardioversion
Haemodynamically stable :
Rate control : If significant tachycardia
Rhythm control : Flecainide, Propafenone (cl-
I) Amiodarone, Sotalol (cl-III)
Anticoagulant : LMWH
21. Treatment for permanent AF
• Heart Rate control
minimise symptoms associated with
excessive heart rates
prevent tachycardia-associated
cardiomyopathy
• Anticoagulation
22. Rhythm control as preferred
therapy
– ? First episode afib
– Reversible cause (alcohol)
– Symptomatic patient despite rate control
– Patient unable to take anticoagulant (falls, bleeding,
noncompliance)
– CHF precipitated or worsened by afib
– ? Young afib patient (to avoid chronic electrical and
anatomic remodeling that occurs with afib)
23. Rate control as preferred therapy
– Age > 65, less symptomatic, hypertension
– Recurrent afib
– Previous antiarrhythmic drug failure
– Unlikely to maintain sinus rhythm (enlarged LA)
24. Cardioversion
• Cardioversion is performed as part of a
rhythm-control treatment strategy
• There are two types of cardioversion:
electrical (ECV) and pharmacological (PCV)
• Cardioversion of AF is associated with
increased risk of stroke in the absence of
antithrombotic therapy.
25.
26. AFFIRM : 5 Year Outcomes
Survival Rhythm Control Rate Control
1 year 96% 96%
3 year 87% 89%
5 year 76% 79%
p = 0.058
NO Difference : death, disabling stroke, major bleed,
or cardiac arrest
Sinus rhythm maintained in only 63% of rhythm
control group
NEJM 2002;347:1825
27.
28. Rate Control Options
• Beta blocker
• Calcium channel blocker
• Verapamil, diltiazem
. Digoxin
• AV junction ablation plus pacemaker
37. ACC AHA HRS Afib Focused Update
(Dabigatran), March 2011
• Non-inferior to warfarin re thromboembolism (afib)
• Caution when CrCl < 30ml/min
• Increased dabigatran levels with amiodarone, verapamil
• Half life 12-17 hours
• No reversal re hemorrhage
– dialysis
• Coagulation testing ??? aPTT, dilute thrombin time
38. Who should remain on warfarin?
• Patient already receiving warfarin and stable whose INR
is easy to control
• If dabigatran, rivaroxaban, apixaban not available
• Cost
• If patient not likely to comply with twice daily dosing
(Dabigatran, Apixaban)
• Chronic kidney disease (GFR < 30 ml/min)
39. Bleeding Risk
• Assessment of bleeding risk should be part of
the clinical assessment of AF patients prior to
starting anticoagulation
• Antithrombotic benefits and potential
bleeding risks of long-term coagulation should
be explained and discussed with the patient
• Aim for a target INR of between 2.0 and 3.0
• Forms of monitoring include point of care or
near patient testing and patient self-
monitoring
42. Substrate for Substrate for
Triggering events
initiation perpetuation
43. When to consider ablation?
• Antiarrhythmic therapy ineffective
• Antiarrhythmic therapy not tolerated
• Symptomatic afib
44.
45.
46. Others in whom ablation may be a first strategy
• Patient very symptomatic in AF and refuses
antiarrhythmic drug therapy
• Young patient whose only effective antiarrhythmic drug
is amiodarone
• Patient with significant bradycardia for whom
antiarrhythmic drug therapy will require pacemaker
47. Summary
• AF is the commonest arrhythmia
• High prevalence
• Stroke is one of the most dreadful
complications .
• Different management strategies,
Editor's Notes
NOTES FOR PRESENTERS Refer to the full guideline – page 13, table 1.01. Renfrew-Paisley UK study, cohort of men and women aged 45-64 years (n = 15,406) there were 100 documented cases of AF. Prevalence of AF increased with age and more cases were detected in men.
NOTES FOR PRESENTERS For more details, refer to the full guideline, pages 11 and 12, section 1.2 AF is considered recurrent when a patient develops two or more episodes. These episodes may be paroxysmal if they terminate spontaneously, defined by consensus as terminating within seven days, or persistent if the arrhythmia requires electrical or pharmacological cardioversion for termination. Successful termination of AF does not alter the classification of persistent AF in these patients. Longstanding AF (defined as over 1 year) not successfully terminated by cardioversion, or when cardioversion is not pursued, is classified as permanent. Without treatment, AF can result in some degree of disruption to the circulation of blood around the body. In some cases of AF, the degree of haemodynamic instability can represent a critical condition that requires immediate intervention. The next slide sets out why we need this guideline.
NOTES FOR PRESENTERS There are many risk factors for developing AF. In the Framingham study, the development of AF was associated with increasing age, diabetes, hypertension and valve disease. It is also commonly associated with, and complicated by, congestive heart failure and strokes. Dietary and lifestyle factors have also been associated with AF, such as excessive alcohol and caffeine, as well as emotional and physical stress. Cardiac causes of AF Common cardiac causes: Ischaemic heart disease Rheumatic heart disease Hypertension Sick sinus syndrome Pre-excitation syndromes (e.g. Wolff-Parkinson-White syndrome) Less common cardiac causes: Cardiomyopathy or heart muscle disease Pericardial disease (including effusion and constrictive pericarditis) Atrial septal defect Atrial myxoma Non-cardiac causes of AF Acute infections, especially pneumonia Electrolyte depletion Lung carcinoma Other intrathoracic pathology (e.g. pleural effusion) Pulmonary embolism Thyrotoxicosis Refer to the full guideline – page 89, section 10 Post-op AF is associated with a greater risk of mortality and morbidity, and evidence is emerging that post-op AF predisposes people to a significantly increased risk of stroke and thromboembolism. The next slide highlights the classification of AF, which is based on the temporal pattern of the arrhythmia.
NOTES FOR PRESENTERS In patients with permanent AF who need treatment for rate-control: - beta-blockers or rate-limiting calcium antagonists should be the preferred initial monotherapy in all patients In patients with permanent AF where monotherapy is inadequate: to control the heart rate during normal activities only, beta-blockers or rate-limiting calcium antagonists should be administered with digoxin to control the heart rate during both normal activities and exercise, rate-limiting calcium antagonists should be administered with digoxin
NOTES FOR PRESENTERS For further details, refer to the NICE guideline – page 27. Patients undergoing PCV are usually admitted to hospital
NOTES FOR PRESENTERS Refer to NICE guideline – pages 22 and 23 In order to provide adequate thromboprophylaxis with minimal risk of bleeding, current clinical practice aims for a target INR of between 2.0 and 3.0; INRs higher than 3.0 are associated with increases in bleeding, and INRs lower than 2.0 are associated with increases in stroke risk.