Atrial fibrillation

Atrial Fibrillation AF is a supraventricular tachyarrhythmia

characterized by uncoordinated atrial activation with consequent deterioration of atrialmechanical function.

A rapid, irregular, sustained, wide-QRS-complex tachycardia strongly suggests AF with conduction over an accessorypathway or AF with underlying bundle-branch block. Extremely rapid rates (over 200 beats per minute) suggest the presence of an accessory pathway or ventricular tachycardia.

Prevalence:

In US <1% ‘ve AF;

Varies with age –

Rare in children & young adults.

Is also rare < 60 yrs.

> 8% in > 80 yrs.

Median age 75 yrs.

Presence of very irregular & disorganized atrial activity

represented - as Fibrillatory waves; aka “F” waves,

These are due to several independent reentrant wavelets

within atria

F waves - fine or coarse ; varying morphologies

F waves may not be present; flat line with irreg irreg R-R

seen.

A. rate - ≥350 bts/min.

V. rate- irreg irreg & depends on # of atrial impulses

conducted through AVN.

QRS complexes are narrow unless - BBB, aberrant

conduction, or preexcitation

Coarse f waves –

RHD MV ds,

Thyrotoxicosis,

Emphysema,

Hypertensive CVD

Fine f waves – Arteriosclerotic hrt dis.

6 Sec time lines:

6 sec = 30 large blocks.

# QRS in 6-sec time X 10= HR/min

1st QRS - not counted; serves as baseline.

10 Sec time lines:

If HR very slow- longer interval -10 sec taken.

10 Sec = 50 large blocks.

# QRS in 10-sec X 6 = HR/min.

AF

Paroxysmal

Persistent

Permanent

Recurrent

First detected: AF detected for 1st time, regardless of

duration or previous episodes.

Recurrent: If >2 episodes ‘ve occurred- may be paroxysmal

or persistent.

Paroxysmal: When recurrent AF has sudden onset & abrupt

termination.

AF that terminates spontaneously or with intervention within 7 d of onset.

Episodes may recur with variable frequency.

Persistent: if AF is >7 days.

Longstanding Persistent AF: continuous AF lasting >1 year.

Not self terminating,

But terminated with pharmacologic/ electrical cardioversion.

Permanent: Permanent AF is used when there has been a joint decision by the patient and clinician

to cease further attempts to restore and/or maintain sinus rhythm.

· Acceptance of AF represents a therapeutic attitude on the part of the patient and

clinician rather than an inherent pathophysiological attribute of the AF.

· Acceptance of AF may change as symptoms, the efficacy of therapeutic interventions,

and patient and clinician preferences evolve.

Nonvalvular AF: in absence of RHD – MV ds, prosthetic

valve, or MV repair.

Valvular AF: - a/w RHD MS, prosthetic valve, or post valve

repair.

Lone AF: AF in age > 60 yrs - with structurally normal hrt,

non HT, no e/o pulmonary dis.

AF -mistaken for SVT:

When V. rate is unusually rapid - R-R interval may

look regular because of very close QRS clustering -

thus mistaken for SVT

Diagnosis of AF ascertained by slowing V. rate with

vagal maneuvers eg- CS pr. – showing irreg-irreg R-

R interval with fibrillatory/ undulating baseline b/w

QRS

AF mistaken for MAT:

F waves, esp when coarse- mistaken for P waves.

When these “F” waves inscribed before QRS- may be

mistaken for MAT

AF with regular R-R intervals:

V. rate in AF is irregularly irregular.

But it becomes regular when there is

complete AV dissociation or

complete AV block.

AF with regular R-R intervals:

Complete AV dissociation:

Frequently due to digitalis toxicity.

Here, V. are no longer controlled by AF, but rather

by separate pacemaker, usually AV jnx with regular

rate > 60 bpm.

AF with regular R-R intervals:

Complete AV Block :

Fibrillatory impulses not conducted to ventricles.

AV junctional/ ventricular escape rhythm usually

comes to rescue

Here V rate is slow & regular- mid to low 40s

Ashman phenomenon:

In AF, R-R intervals are irreg-irreg.

Some R-R are longer & other shorter.

When R-R increased, HR is decreased, RP of

conduction tissues becomes increased.

When R-R decreased or HR increased, RP is

decreased.

Ashman phenomenon:

If long R-R is f/b short R-R (long/short cycle), atrial

impulse may find RBB still refractory from previous

impulse & will conduct with wide QRS.

This aberrantly conducted complex is 2nd complex

(complex with short cycle following long cycle).

This variability in RP is k/a Ashman phenomenon

Atrial fibrillation & WPW Sx

WPW Sx – Impulses from A to V via AVN + AP.

Unlike AVN, which has >RP; AP has much <RP.

Thus, during AF, rapid A. impulses that are delayed/

blocked at AVN d/t its > RP, are conducted via AP,

resulting in very rapid V rate.

Atrial fibrillation & WPW Sx

AVN blocking agents are standard drugs for

controlling V. rate in AF.

H/e These are C/I in WPW sx - they enhance

conduction across AP resulting in rapid V rate &

hemodynamic collapse

Pathophysiological Mechanisms

Atrial Pathology as a Cause of Atrial Fibrillation The most frequent patho anatomic changes in AF are

atrial fibrosis and loss of atrial muscle mass.

Patientswith mild or moderate fibrosis responded more successfully tocardioversion than did those with severe fibrosis, which was thought to contribute to persistent AF in cases of valvularheart disease

Atrial fibrosis may be caused by genetic defects like lamin AC gene mutations . Other triggers of fibrosis include inflammation as seen in cardiac sarcoidosisand autoimmune disorders.

Autoimmune activity is suggested by high serum levels of antibodies against myosin heavy chains in patients with paroxysmal AF who have no identified heart disease

Fibrosis is also triggered by atrial dilation in any type of heart disease associated with AF, including valvulardisease, hypertension, HF, or coronary atherosclerosis.

Stretch

RAAS

TGF-beta1

connective tissue growth factor

Fibrosis

Transition of AV reentry into AF in patients with the Wolff-Parkinson-White (WPW) syndrome can produce a rapid ventricular response that degenerates into ventricular fibrillation, leading to death .

Intravenous administration of drugs such as digitalis, verapamil, or diltiazem, which lengthen refractoriness and slowconduction across the AV node, does not block conduction over the accessory pathway and may accelerate the ventricular rate.

A, Focal activation. The initiating focus (indicated by the star) often lies within the region of the pulmonary veins. The resulting wavelets represent fibrillatoryconduction, as in multiple-wavelet reentry.

B, Multiple-wavelet reentry. Wavelets (indicated by arrows) randomly reenter tissue previously activated by the same or another wavelet.

Etiologies and Factors Predisposing Patients to AF

Atrial Fibrillation

-- Prevalence in associated diseases --

Hypertension – increased relative risk of only 1.42; however prevalence of hypertension accounts for the high association

CAD – AF is transient in 6-10% of MI patients; however it is almost never in isolation to other ECG findings of ACS (Zimetbaum et al. Incidence and

predictors of myocardial infarction among patients with atrial fibrillation. J Am Coll Cardiol 2000; 36;1223)

Incidence in chronic, stable CHD is 0.6%

Valvular heart disease

High prevalence with Rheumatic heart disease

MS + MR – 52%

MS alone – 29%

MR alone - 16%

AS alone – 1%

Degenerative MR incidence 5% per year

Atrial Fibrillation-- Prevalence in associated diseases, cont. --

Heart Failure – 10-30% Pulmonary embolism – 10-14 % (rarely the only sign or

symptom) Hyperthyroidism – low TSH in 5.4%; clinical

hyperthyroidism present in 1% COPD Post cardiac surgery Pericarditis Obstructive sleep apnea ( for patients with AF and OSA, incidence of AF

recurrence is 2X for those not treated with CPAP)

Congenital heart disease Peripartum cardiomyopathy “Holiday Heart”

Atrial Fibrillation-- Pathogenesis --

Underlying heart disease of any cause that is complicated by: heart failure atrial enlargement elevated atrial pressure inflammation or infiltration of the atria

Echocardiographic risk factors increased left ventricular wall thickness left atrial diameter > 4 cm reduced left ventricular fractional shortening

Triggering event majority related to atrial premature beat minority related to atrial flutter or atrial tachycardia

Atrial Fibrillation-- Management and Disposition --

Which category? Recent onset AF

Recurrent paroxysmal AF

Recurrent persistent AF

Permanent (Chronic) AF

and patient condition, determines

Which primary option Rate control

Urgent cardioversion

Delayed cardioversion

Rhythm control / maintenance if converted

Systemic embolization prevention

Atrial Fibrillation-- Management and Disposition --

“Elective” cardioversion in the ED duration clearly identified less than 48 hrs

No reversible cause

low risk of intra-cardiac thrombus formation

Atrial Fibrillation-- ED Cardioversion in the stable patient --Burton, John H. et al. Electrical cardioversion of ED patients with Atrial

Fibrillation. Annals of Emergency Medicine 2004;44: 22-30

Retrospective, consecutive cohort

42 months,

Oct 1998 – March 20024 institutions

3,688 AF encounters

Excluded: Cardioversion for unstable patientshypotension, dyspnea, ischemic chest pain, alteredconsciousness, CHF, acute MI

No standardized protocol at any of the study sites

388 stable AF encounters(10.5%)

Mean age = 61 +/- 13 yrs

332 successful (86%)

56 unsuccessful (14%)

91% discharged

55% discharged

9% admitted

45% admitted

Atrial Fibrillation-- Management and Disposition --

“Urgent” or “Emergent” cardioversion in the ED

What are the indications?

What are the contraindications?

Atrial Fibrillation-- Management and Disposition --

Urgent cardioversionRestoration of sinus rhythm takes precedence over mitigation of thromboembolic riskIndicated if any of the following is present:• Active ischemia• Significant hypotension where LV dysfunction (systolic or diastolic) or valvular

disease is a factor• Severe CHF • Pre-excitation syndrome (eg WPW)

“Relative” Contraindications to urgent cardioversion Duration of episode > 48hrs or uncertain duration Associated mitral valve disease, cardiomyopathy or CHF (known EF < 50%) Prior history of thromboembolic event

Rate V Rhythm control first?RateOver 65

Coronary artery disease

Unsuitable cardioversion

Unsuitable for antiarrhythmics

RhythmUnder 65

Lone AF

CCF

Secondary to treated trigger

Paroxysmal AF

Rate control

Atrial Fibrillation-- Antiarrhythmic agents --

Fast Channel (Na+)Action Potential

Purkinje fibers

Slow Channel (Ca++)Action PotentialSinus / A-V Nodes

0

1

2 3

4

2

0

Myocardial Cellular Electrophysiology

Class 1 antiarrhythmics-Slowing of conductance-Phase 0 is determined by Na+ channel-Slowing of conduction velocity

and decreased excitability

Class 4 antiarrhythmics-Slowing of AV nodal conductance-Phase 0 is determined by Ca++ channel-Slowing of conduction velocity in

sinus and AV nodes

-- Antiarrythmic Agent Classification—Vaughn-Williams Classification (Journal of Clinical Pharmacology, 1984)

Class 1- depression of Na+conductance during phase 0; slowed conduction velocity and decreased excitability

1a: moderate depression of Na+ conductance in resting and depolarized tissue; depression of K+ currents and prolongation of repolarization

Quinidine, Procainamide, Disopyramide

1b: depression of Na+ conductance in depolarized fibers only; Lidocaine, Tocainide, Phenytoin

1c: marked depression in Na+ conduction; no effect on repolarization Encainide, Flecainide, Propafenone

Class 2- β-adrenergic receptor blockers

Atenolol, Metoprolol

Class 3- prolongation of action potential duration by varied effects Bretylium, Sotolol, Amiodarone, Ibutilide, Dofetilide

Class 4- depression of Ca+-dependent slow channels Diltiazem, Verapamil

Atrial Fibrillation-- Management and Disposition --

Delayed cardioversion

AF duration of 48 hours or duration unknown

Associated mitral valve disease, cardiomyopathy or CHF

Prior history of thromboembolic event

Anticoagulate with a goal INR of 2.0 to 3.0 for at least three weeks before and four weeks after either electrical or pharmacologic cardioversion.

Atrial Fibrillation-- Management and Disposition for Delayed ECV -- Strategy 1 (Conventional)

Oral anticoagulation with Warfarin Target INR 2.0 – 3.0

No antiarrythmics Rate control as needed – hospitalization usually necessary if rate control needed

Metoprolol Diltiazem Digoxin (useful only in presence of CHF)

Scheduled ECV after minimum of 3 weeks of anticoagulation 4 weeks of anticoagulation after ECV

Strategy 2 Indication

recent onset but > 48 hrs useful for hospitalized patients (rate control, associated complications) and stable patients for

which earlier timing is useful Patients with increased risk of hemorrhage with anticoagulation

Screening Transesophageal echocardiography (TEE) No anticoagulation No antiarrhythmics Rate control as needed

ECV if no thrombi seen

Atrial Fibrillation

-- Indications for hospitalization --

For the treatment of an associated medical problem, which is often the reason for the arrhythmia

For elderly patients who are more safely treated for AF in hospital

For patients with underlying heart disease who have hemodynamic consequences from the AF or who are at risk for a complication resulting from therapy of the arrhythmia

Atrial Fibrillation-- Rate control alone vs rhythm control--Rhythm control strategy

Advantages: Better exertional capacity Improved cardiac function for CHF patients Mitigation of other arrhythmic related symptoms (eg palpitations)

Disadvantages: frequent recurrences of AF – 50% of patient recurr in 3-6 months repeated need for electrical cardioversion; adverse effects of prophylactic antiarrhythmic drugs including life-threatening

events related to proarrhythmic effects

No clear benefit of either approach for patients over 65 years of age; trend for increased mortality in rhythm control (AFFIRM trial, NEJM 2002, > 4,000 patients)

Rate control with anticoagulation is acceptable in patients 65 yrs or greater

Strategy is weighed for acutely symptomatic patient with new onset of Atrial fibrillation, particularly if < 65 yrs

Atrial Fibrillation-- Rate control alone vs rhythm control --

VanGelder, et al, A Comparison of Rate Control and Rhythm Control in Patients with Recurrent Persistent Atrial Fibrillation, NEJM 2002;347:1834-40

522 Patients with persistent AF after

previous electrical cardioversion

Mean age 68 +/- 8

Mean duration of AF diagnosis 315 d

Mean duration of presenting episode 32 d

No history of heart disease 21%

Primary Endpoints: DeathCHF TE event BleedingPacersevere drug adverse event

Primary endpoint:Rhythm control = 23%Rate control = 17%

Follow up period of at least 2 yrs

Rhythm control Rate control

Entry: ECV + Sotolol

1st recurrence: ECV + Flecanide or Propafenone

2nd recurrence: Amiodarone load +ECV + Amiodarone main.

Target HR < 100Digoxin, Diltiazem,

β blocker – alone orIn combination

All patients anticoagulated: could be discontinued ifIn NSR 4 weeks after ECV

Atrial Fibrillation-- Rate control alone vs rhythm control --

VanGelder, et al, A Comparison of Rate Control and Rhythm Control in Patients with Recurrent Persistent Atrial Fibrillation, NEJM 2002;347:1834-40

Factors related to lack of risk reduction with rhythm control strategy

•Tachycardia induced cardiomyopathy and heart failure also are likely reduced with rate control (incidence of CHF similar inthe two arms of the study)

•Patients with risk factors for stroke are still at risk for stroke evenwhen sinus rhythm is maintained (17% of the thromboembolicevents occurred after cessation of anticoagulant therapy and in5 of 6 cases the patient was in sinus rhythm at the time of the event)

•Senescent conduction disease is occasionally unmasked by rhythm control strategy

Atrial Fibrillation-- Maintenance of Sinus Rhythm after Chemical or Electrical Cardioversion --

Canadian Trial of Atrial Fibrillation Investigators

Roy, et al Amiodarone to Prevent Recurrence of Atrial Fibrillation, NEJM, 2000;342:913-920

403 patients; 19 centers

201 Amiodarone 202 Propafenone ; Sotolol

101 Propafenone 101 Sotolol

Mean 16 month follow-up

35% recurrence for Amiodarone 63% recurrence for Propafenone or Sotolol

Atrial Fibrillation-General Management Principles--- Pharmacologic Cardioversion -- Semi – urgent (hospitalization or Obs Unit)

Class 1c used only if no pre-existant heart disease monitoring for rapid conducting At. Flutter

Flecainide Propafenone

Class 3 monitoring for QT prolongation; Torsade

Dofetilide Ibutilide

Out-patient / Ambulatory scenario Class 1c “Pill-in-the-Pocket”

Flecainide Propafenone Used only when demonstrated effective under as in-patient Must have AV nodal blockade with β blockade or Ca++ channel blocker to prevent 1:1

AV conduction if Atrial flutter occurs

Class 1c Extended dosing Amiodarone –particularly with patients with pre-existing heart disease

Atrial Fibrillation-General Management Principles--- Maintenance of Sinus Rhythm after Chemical or Electrical Cardioversion –ACC / AHA / ESC anticoagulation recommendations

Atrial Fibrillation-General Management Principles-

Assessment of Thromboembolic Risk

Atrial Fibrillation-- Risk for Thromboembolism --

Go, AS, Hylek, EM, Chang, Y, et al, JAMA 2003

Risk assessment – CHADS2

CHF – any history (1)

Hypertension – prior history (1)

Age > 75 (1)

Diabetes mellitus (1)

Stroke, TIA or systemic embolic event (2)

Atrial Fibrillation-- Risk for Thromboembolism --

Risk assessment – CHADS2

Go, AS, Hylek, EM, Chang, Y, et al, JAMA 2003

Score (risk) Event rate (% / yr)

Warfarin Without Warfarin NNT

0 (low) 0.25 0.49 417

1 (interm) 0.72 1.52 125

2 (interm) 1.27 2.50 81

3 (high) 2.2 5.27 33

4 (high) 2.35 6.02 27

5,6 (high) 4.6 6.88

Atrial Fibrillation-- Prevention of Thromboembolism --

ACC / AHA / ESC anticoagulation recommendations

Age < 60 + heart disease but no other risks: Aspirin

Age 60 – 75 with no risks: Aspirin

Age 65 – 75 with heart disease or DM: Warfarin

Women > 75: Warfarin

Men > 75: Warfarin or Aspirin

Age > 65 with CHF: Warfarin

EF < 35% + Hypertension Warfarin

CHA2DS2-VASc acronym

Congestive HF

Hypertension

Age ≥75 y

Diabetes mellitus

Stroke/TIA/TE

Vascular disease (prior MI, PAD, or aortic plaque)

Age 65–74 y

Sex category (i.e., female sex

Maximum Score

1

1

2

1

2

1

1

1

9

Risk-Based Antithrombotic Therapy: Recommendations

Atrial Fibrillation-- Summary –

Patients with new onset atrial fibrillation of less than 48 hrs duration, who have normal ventricular function, no known mitral valvular disease and no history of thromboembolic event can be considered for cardioversion in the ED

Up to 90% of atrial fibrillation episodes are asymptomatic with approximately 20% of such episodes longer than 48 hrs (Select your cardioversion cases carefully!)

If the episode is greater than 48hrs, rate control, anticoagulate and refer for delayed cardioversion

TSH and free T4 are essential in the evaluation of initial onset AF is transient in 6-10% of MI patients; however it is almost never in

isolation to other ECG findings of ACS AF is transient in 6-10% of MI patients; however it is almost never in

isolation to other ECG findings of ACS

The following are 10 points to remember about the 2014 guideline for the management of patients with nonvalvular atrial fibrillation (AF):

1. In assessing risk of stroke in a patient with nonvalvular AF, the writing committee recommends (Class I) the usage of the CHA2DS2-VASc (C=congestive heart failure; H=hypertension; A2=age ≥75 years [doubled]; D=diabetes mellitus; S2=stroke, transient ischemic attack, or thromboembolism [doubled]; V=vascular disease; A=age 65-74 years; Sc=sex category, i.e., female gender) score, as opposed to the CHADS2 score.

2. For nonvalvular AF patients with a history of stroke or transient ischemic attack, or a CHA2DS2-VASc score ≥2, oral anticoagulation is recommended (Class I). Options for oral anticoagulation include warfarin, dabigatran, rivaroxaban, and apixaban.

3. For patients with nonvalvular AF and a CHA2DS2-VASc score of 0, it is reasonable to omit antithrombotic therapy (Class IIa).

4. The following options may be considered with a patient with nonvalvular AF and a CHA2DS2-VASc score of 1: no antithrombotic therapy, oral anticoagulation, or aspirin (Class IIb).

5. None of the novel oral anticoagulants (dabigatran, rivaroxaban, or apixaban) are recommended to be used in patients with AF and a mechanical or bioprosthetic heart valve (Class III harm).

6. As in the earlier guidelines, the committee recommends against the use of certain antiarrhythmic medications (flecainide, propafenone, dofetilide, and sotalol) in patients with severe left ventricular hypertrophy (LVH). In the current guidelines, severe LVH is now defined as wall thickness exceeding 1.5 cm.

7. Oral anticoagulation should be prescribed to patients with hypertrophic cardiomyopathy and AF irrespective of the CHA2DS2-VASc score (Class I).

8. A randomized trial suggested that a lenient (<110 bpm) rate control strategy was as effective as a strict strategy (<80 bpm) in patients with persistent/permanent AF. However, the writing committee still advocates for the latter (Class IIa), as the results of this single trial were not thought to be definitive.

9. Catheter ablation is useful in patients with symptomatic, paroxysmal AF who have not responded to or tolerated antiarrhythmic medications (Class I).

10. Catheter ablation is also reasonable in selected patients with symptomatic, paroxysmal AF prior to a trial of medical therapy, provided that it can be performed at an experienced center (Class IIa).

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