ATRIAL FIBRILLATION

…..Grand father of arrhythmias

The most essential part of a student's instruction is obtained...not in the lecture-room, but at the bedside. Nothing seen there is lost; the rhythms of disease are learned by frequent repetition; its unforeseen occurences stamp themselves indelibly in the memory.

o - Oliver Wendell Holmes, M.D.

Professor: define seminar

Student :seminar is defined as process in which one spoils his sleep for one night in an effort to make others sleep.

ARRYHTHMIAS

For an arryhthmia to occur,to be sustained.Either of three properties to be present. 1.TRIGGERING ACTIVITY OF FOCUS 2.AUTOMATICITY 3.REENTRY In AF all three play a role In AFL – reentry circuit. WAVELETS SPIRAL WAVE

What is triggering?

Triggering is a phenomenon due to cellular afterdepolarization.

1.at end of AP during phase 3 –early AD 2.after AP –phase 4 –late AD Increases in intracellular Ca VPC –TDP early after DP Late after DP- atrial,ventricluar ,facicular dysarrhythmias

due to digoxin toxicity. Catecholamine response VT --- late AD Provoked by pacing

Action potential

Foci of excitation in AF

What is automaticity?

Due to increase in the slope of phase 4 depolarization. Decreased threshold for AP depolarization in myocardium

other than sinus node. Most of APCs VPCs AT Cannot be provoked by pacing

What is reentry?

Inhomogenous in myocardial conduction and recovery. Unidirectional block with slow conduction• WPW. Fibrosis ---SVTs,VTs FIXED– crista terminalis,vertical crest on the inferior wall of

right atrium. Functional dynamic --- unstable-• VF –acute MI • Polymorphic VT

REENTRY

AVNRT

Wavelets in AF

SPIRAL WAVE

Functional rentrant circuit. The centre of reentry is excitable but not activated. Latest model of AF Still not clearly understood

What is pacing?

DELIVERING THE PULSES Treatment in case of SSS And also to suppress the tachyarryhthmias

1 2 3 4 5

Chamber paced

Chamber sensed

Response to sensing

Rate modualtion

Multisite pacing

A A T O O

V V I R A

D D D V

O O D

What is overdrive suppression?

OVERDRIVE SUPPRESSION is the phenomenon in which the rate of the pacemaker decides the ryhthm over the underlying other cells..

One which is at a faster rate will be the pacemaker.. Others will not give impulses of their own and are

suppressed –overdriven by the pulse of other one.. Normally all other pacemaker cells are overdriven by siuns

node. Sometimes SA node may be overdrive n by ectopic foci—

tachycardia.

ATRIAL FIBRILLATION

…..Grand father of arrhythmias

History• Earliest record of AF –yellow emperor ‘s classic of

internal medicine in 17 th century.• WILLIAM HARVEY---auricular fibrillation in animals

in 1628.• Pulse tracing of a patient with AF---Chauveau and

Marey• First clinical case of AF after surgery of ovarian tumor

–Arthur Cushy in london,1907.• Rebellious palpitation ---Jean Baptiste Senae• Absence of p waves---Lewis• Irregular pulse of AF--- “intermssion of pulsation of heart”--Laennec ‘Ataxia of pulse’– Bouilland ‘Delirium cordis’—Nothnagil ‘Pulsus Irregularis Perpetius’--- Hering

Micheal Haissaguerre

• Showed that AF can be initiated by ectopic beats originating in the pulmonary veins and that ablation of these sites are curative

CLASSIFICATION OF A F

• Temporal classification clinically.• Why?---management strategy changes.• Individualised –h/o, compliance ,other disorders.• ACC/AHA/ESC 2006 GUIDELINES ETIOLOGICALLY — NON VALVULAR AF—abs of RHD,MVR,prosthetic valve VALVULAR AF--- presence LONE AF. CLINICALLY FIRST EPISODE TRANSIENT AF/REVERSIBLE AF RECURRENT AF• PAROXYSMAL AF• PERSISTENT AF PERMANENT AF

LONE AF

To be categorised as lone AF ,it is after exclusion of other factors.

1.age <60 yrs 2.absence of heart disease or pulmonary disease 3.non hypertensive 4.no clinical or echocardiographic evidenceo 20-25% of persistent AF Why imp? Low risk of thromboembolism Can be kept on plain aspirin 81-325 mg daily. Trials--- paris prospective study RR of CV mortality ---4.22

%total mortality --- 1.97 %

FIRST EPISODE AF—symptomatic or asymptomatic revert to SR spontaneously in most patients.

RECURRENT AF--- 2 or more episodes occurred.> 30 sec

PAROXYSMAL AF– recurrent AF that ends spontaneously <48 hrs – 7 days .

PERSISTENT AF --- > 7 days . Requires pharmacotherapy or cardioversion for termiantion

PERMANENT AF --- Cannot be reverted.

REVERSIBLE/TRANSIENT AF----ac URTI, AMI,pericarditis,thyrotoxicosis,pulmonary embolism,after CABG,holiday heart syndrome.

EPIDEMIOLOGY

Incidence in age >22 yrs –2% --- FRAMINGHAM study. M>W 0.5% prevalence 50-59 yrs,,8.8%--80-89 yrs Increases with age. SAFE STUDY–MEN—7.8% overall,elderly -10.8% West brimingham AF project—HTN—37%,IHD—29% Lifetime risk @ 4o yrs –26% in men ,23% in women—

FRAMINGHAM STUDY. Relative risk for death –1.5 in men ,1.9 in women—no

age influence. PAROXYSMAL- >>>>>>>PERMANENT---8% per yr

ETIOLOGY

CARDIAC 1.HYPERTENSION 2.VALVULAR HEART DISEASE 3.CORONARY HEART DISEASE 4.CARDIOMYOPATHY 5.CONGENITAL HEART DISEASE 6. CARDIAC SURGERY 7.ELECTRICAL DISEASE—SINUS NODE

DYSFUNCTION,TACHY INDUCED,FAMILIAL 8.PERICARDIAL DISEASES 9.GENETIC

NON CARDIAC ENDOCRINE--THYROID DISEASE TOXIC SUBSTANCE—ALCOHOL AUTONOMICALLY MEDIATED PULMONARY DISEASE NEUROLOGICAL IDIOPATHIC

PATHOPHYSIOLOGY

• still a clear picture of pathophysiology is not known.• Several mechanisms were put forward based on etiology.• What actually initiates is not known..• What makes an ectopic to trigger?

For an AF to occur 1.diseased atria 2.susceptible substrate 3.triggering foci 4.sustained activity of that trigger 5.reentry circuits electrically 6.structural remodelling 7.wavelets formation

Sympatho vagal discharges--- Ca release from SR in diastole---early .delayed after depolarisation----- ectopic activity--- presence of susceptible substrate– AF

REENTRY depends on balance between cellular refractoriness and conduction speed.

refractory period decreased,slow conduction---continuous conduction in a potentially reentry zone electrically---LEADING CIRCLE THEORY..

Around central core--- rapidly circulating roto with a wave front .size of wave depends on tissue excitability and refractoriness--- SPIRAL WAVE THEORY..

CONTINUED…AF BEGETS AF

TRIGGER --- AF ----increased atrial rate --- decreased AP duration ----- decreased effective refractory period --- cycle of reentry continues --- atria gets habituated electrically ---- ---- electrical remodelling – increased sustained reentry--- AF

AF BEGETS AF

This explains all the categoristion of AF Paroxysmal -- trigger present , not sustained Persistent --- electrical remodelling occurred. Permanent ---- cellular remodelling occurred.

dobrev.d HERZ 2006 : 31: 108-12

duytschaever--- drugs action after remodelling,cardiac res. 2005 ;67-69

burstein –atrial fibrosis –JACC 2008

Pressure overload,volume overload ---- atrial enlargement --due to stretch activated channels intracellular acidosis---AF.

Where is the trigger coming from/ Sleeves of atrial myocardium extending into

pulmonary veins. SVC Vein of marshall Coronary sinus

haissaguerre m NEJM 1998

REENTRANT ARRHYTHMIA----- JACC 2004

electrophysiology

A.multiple wavelet reentry- Sweep through atrium in random fashion >5 to 6 Enough atrial tissue to be present for propagation. B.1 rentrant circuits or rotors- Constant forming and disappearing Cycle length too short C.musculature of pulm vein,posterior left atrial

wall Reentrant excitation

ATRIAL REMODELLING

ELECTRICAL STRUCTURAL

abnormal conduction of impulse Structure is changed for disorganised conduction of impulse

L type Ca current Collagen synthesis

AERP Fibrosis around PVS and posterior LA wall

loss of rate adaptive AERP shortening

De differentiation of atrial cells

Conduction velocity Inflammatory cells

Sinus node dysfunction Amyloid deposits

Apoptosis

necrosis

Abnormal conduction

AF IN HYPERTENSION MC cause in developed countries. 50 % cases. HTN– reduced LV compliance ---- LA dilation ---- AF HTN ---- CAD ---- AF -- THROMBO EMBOLISM “ increasing pulse pressure is a strong predictor of

subsequent AF”------------------------------ -Crawford More risk of stroke . Given a score of 1.

In CAD – Infrequent In Ac MI --- early phase 10- 15 % cases. a marker of poor prognosis earlier …. Self limited

AF IN ALCOHOLICS

Acute and chronic alcohol ingestion. 60% of binge drinkers regardless of presence of

alcoholic cardiomyopathy. Episode of AF after heavy alcohol ingestion ---holiday

heart syndrome. Chronic alcohol---- htn,cardiomyopathy---- HF ---- AF

AF IN THYROID DISORDERS

20-25 % of older patients. Uncommon in < 30 yrs Serum free thyroxine concentration ---independently

assosciated with AF. Digoxin alone cannot control the heart rate. B blockers are drug of choice Usually transient. Cardioversion not to be attempted until normo

thyroid..

AF IN CARDIOMYOPATHY 28% of HOCM Reversible after cardioversion ,ventricular rate control

. 20 % of DCM Mild to moderate --- no change in mortality. Advanced HF – SCD

Genetic causes 4 genes --- k channel subunits Shortening of AP Decreased atrial effective refractory period DNA polymorphisms

AF post operative

20- 40 % of CABG 2-8 th postoperative days Who are at risk Elderly Prev h/o of AF RCA stenosis B blockers discontinued preoperatively. Left atrial volume --- strong ,independent predictor of

post op AF. CRAWFORD

AF IN RHD

MS --- 29% MR 16 % TR MS with MR --- 52 % In AS with HF If a patient in MS had AF ---- risk of stroke is 3-7

times than that of in NSR . All patients to be anticooagulated.

Clinical features

Asymptomatic Triggers—fever ,chest infection , HTN , HF

minor major

Palpitations CHF

fatigue ANGINA

Light headed ness HYPOTENSION

PRESYNCOPE

SYNCOPE

WHEN SYNCOPE OCCURS,SUSPECT?

Pre excitation Increased AV CONDUCTION Sinus node disease---sinus arrest HOCM AS

• Apex pulse deficit• BP average of three• Hypotension or normal or hypertensive

Diagnosis

ECG 2D ECHO HOLTER MONITORING—PAROXYSMAL EXERCISE STRESS TEST- IHD CATHETERISATION –BEFORE ABLATION THYROID FUNCTION TESTS IN ALL. Chest x ray Fasting lipid profile

ECG of AF

Evaluation of AF based on ECG

Very irregular ,disorganised atrial activity– fibrillatory waves.

F waves– several independent re entrant wavelets within atria.

Fine or coarse May be flat line between R-R complexes AR . 350 -500 bpm VR --- irregularly irregular , conduction of AV NODE. How are QRS complexes/ Narrow/broad Broad--- BBB, aberrant conduction ,pre excitation HR calculation– 6 second time lines—6*10

How do you differentiate?

In case of FVR to differentiate from SVT Carotid sinus pressure The R-R interval increases ---undualting base line.

From MAT ---- coarse waves of AF taken as P waves .o P waves do change in MAT ..not so in AF.

Regular R-R intervals in AF – implanted ventricular pacemakers. Complete AV dissosciation ---- 60 bpm Complete AV Block ---- 40 bpm Digitalis toxicity From PVC s

ASHMANN PHENOMENON

Long R- R interval is followed by short R- R intervals. Atrial impulse may find the RBBB still refractory.. Wide QRS complexes. Complex with a short cycle following long cycle is

called ashmann phenomenon. How you diff--- lack of compensatory pause.

AF with WPW

Shorter refractory period in specialised cells of abnormal pathway..

They don’t have refractory period of 0.35 seconds as in AV NODE.

So there will be a fast ventricular rate. What is the imp? AV NODAL blocking drugs are contraindicated. SCD

2d echo

see for left atrial size.. Normal is less than 4 cm in

adults. Early marker of uncontrolled

hypertension. Check for valvular lesions Check for left ventricular end

diastolic volumes.

Cardiac catheterisation ---- pacemaker implantation

Holter monitoring ---- paroxysmal events..

stress testing in case of IHD. Stress testing for CVR.

DIFFERENTIAL DIAGNOSIS

1.AFL 2.MULTIFOCAL ATRIAL TACHYCARDIA. 3.ATRIAL PREMATURE COMPLEXES 4.SINUS TACHYCARDIA 5.VENTRICULAR TACHYCARDIA 6.VENTRICULAR FIBRILLATION

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