1. Dr. Jamal Dabbas Interventional cardiologist & internist
Atrial Fibrillation
Dr. Jamal Dabbas
Interventional cardiologist & internist

3. Some types of arrhythmia
Supraventricular
Sinus Nodal
Sinus bradycardia
Sinus tachycardia
Sinus arrhythmia
Atrial
Atrial tachycardia
Atrial flutter
Atrial fibrillation
AV Nodal
AVNSVT
Heart blocks
Junctional
Ventricular
Escape rhythms
Ventricular tachycardia
Ventricular fibrillation

4. Atrial fibrillation
A heart rhythm disorder (arrhythmia). It usually involves a rapid heart rate, in which the upper heart chambers (atria) are stimulated to contract in a very disorganized and abnormal manner.
A type of supraventricular tachyarrhythmia
The most common arrhythmia

6. Aetiology Rheumatic heart disease Coronary heart disease (MI)
Hypertension
Myopericarditis
Hypertrophic cardiomyopathy
Cardiac surgery
Thyrotoxicosis
Infection
Alcohol abuse
Pulmonary embolism
Caffeine
Exercise
Lone AF

7. Classification New / Recent onset Paroxysmal Persistent Permanent
< 48 hours
Paroxysmal
variable duration
self terminating
Persistent
Non-self terminating
Cardiovertable
Permanent
Non-cardiovertable

8. Symptoms / Signs Breathlessness / dyspnoea Palpitations
Syncope / dizziness
Chest discomfort
Stroke / TIA
6 x risk of CVA
2 x risk of death
18 x risk of CVA if rheumatic heart disease
Irregularly irregular pulse
Atrial rate
bpm
Ventricular rate depends on degree of AV block
bpm
Peripheral rate slower (pulse deficit)

9. Investigations Electrocardiogram (ECG)
All patients
May need ambulatory monitoring
Transthoracic echocardiogram (TTE)
Establish baseline
Identify structural heart disease
Risk stratification for anti-thrombotic therapy
Transoesophogeal echocardiography (TOE)
Further valve assessment
If TTE inconclusive / difficult

10. Normal Sinus Rhythm

11. ‘Fast’ AF

12. ‘Slow’ AF

13. Investigations Electrocardiogram (ECG)
All patients
May need ambulatory monitoring
Transthoracic echocardiogram (TTE)
Baseline
Structural heart disease
Risk stratification for anti-thrombotic therapy
Transoesophogeal echocardiography (TOE)
Further valve assessment
TTE inconclusive / difficult

14. Diagnosis
Based on:
ECG
Presentation
Response to treatment

15. Treatment objectives
Rhythm / rate control
Stroke prevention

16. Treatment strategies New / Recent onset Cardioversion Rhythm control
Paroxysmal
Rate control or cardioversion during paroxysm
Rhythm control if needed
Persistent
Cardioversion
Rhythm control
Peri-cardioversion thromboprophylaxis
Permanent
Rate control
Thromboprophylaxis

17. Pharmacological Options
Class Ic Anti-arrhythmics
Flecainide / Propafenone
Rhythm control
May also be pro-arrhythmic
Class II Anti-arrhythmics
Beta-blockers
Mainly rate control
Control rate during exercise and at rest
Generally first choice
Choice depends on co-morbidities
The standard classification of antiarrhythmic drugs is Vaughn-Williams. This is based on the effect of the drugs on the action potential. Digoxin is not included.
All classes have a place in the management of AF. Choice depends of type of AF, co-morbidities and other patient factors.
The Class Ic antiarrhythmics are used to restore and maintain sinus rhythm. They are, however, negatively inotropic (shouldn’t be used in heart failure) and are also pro-arrhythmic, especially if the patient has coronary heart disease.
The Class II anti-arrhythmic drugs are the beta-blockers. Mainly used for rate control, and are effective both at rest and during periods of high sympathetic tone e.g. exercise, stress. They are usually first choice unless contra-indicated, e.g. asthma, acute heart failure.

18. Class III Anti-arryhthmics
Amiodarone / Dronedarone
Mainly rhythm control
May be pro-arrhythmic
Concerns over toxicity
Class IV Anti-arryhthmics
Calcium channel blockers (verapamil / diltiazem only)
Rate control only
Alternative to beta-blockers if no heart failure
Digoxin
Does not control rate during exercise
Third choice unless others contra-indicated
The class III agents are amiodarone and dronedarone, although sotalol, a beta-blocker also has class III effects. They work by prolonging the action potential and therefore both restore and maintain sinus rhythm. Amiodarone is particularly effective but its long term use is limited by serious side effects. Dronedarone is a newer, less toxic but less effective alternative. It’s use is limited in patients with heart failure and there are now concerns about hepatotoxicity.
Intravenous amiodarone is useful to restore sinus rhythm in acute AF.
The Class IV antiarrhythmics are the calcium channel blockers verapamil and diltiazem. They are useful alternatives to beta-blockers but are contra-indicated in acute and chronic heart failure.
Digoxin has been used for hundreds of years. It is of little use in patients who are active since high sympathetic tone overcomes its effect at the AV node. Its main role is in rapid rate control in patients who also present in acute heart failure and in those patients who require long-term management but lead sedentary lifestyles.
Plasma levels need to be checked due to a narrow therapeutic index.

19. Acute AF Treatment will depend on: History of AF
Time to presentation (<> 24 hours)
Co-morbidities (CHD, CHF/LVSD etc)
Likelihood of success (History)

20. Rhythm control not feasible or safe
Rate Vs. Rhythm control
Rhythm control not feasible or safe
Beta-blocker
Verapamil
Digoxin (CHF)
Rhythm control if possible and safe
DC cardioversion (if possible)
Amiodarone (CHD or CHF/LVSD)
Flecainide (Paroxysmal AF)

21. Paroxymal AF Rhythm control* Beta-blocker Class 1c agent or sotalol
If CHD - sotalol
If LVD: Amiodarone
Dronedarone?
Not if heart failure
*May be “Pill in the pocket”
Antithrombotic therapy as per risk assessment
Aspirin mg
warfarin to INR 2-3
See later

22. Persistent AF Rhythm control Beta blocker
No structural heart disease: Class 1c* or sotalol
Structural heart disease: amiodarone
Rate control
As for permanent AF
* not if CHD present
Antithrombotic therapy as per risk assessment
Pre-cardioversion thromboprophylaxis of at least 3 weeks
If rate control, as for permanent AF

23. Permanent AF Beta blocker or Calcium channel blocker and/or Digoxin
Amiodarone?
Option if poor rate control on above
Dronedarone?
Increased mortality
Antithrombotic therapy as per risk assessment
Aspirin mg
Warfarin to INR 2-3
See later

24. Stroke Risk Assessment (CHADS2)
C Chronic Heart Failure (1 point)
H Hypertension (1 point)
A Age > 75 years (1 point)
D Diabetes (1 point)
S Stroke, TIA or systemic embolisation (2 points)
Score < 2: low risk, aspirin* or anticoagulant
Score ≥ 2: high risk, anticoagulant indicated
*Evidence for aspirin is weak
The choice of anticoagulation versus antiplatelet therapy to reduce the risk of stroke is based on the balance between the stroke risk versus the risk of a serious bleed.
The CHADS2 scoring system is commonly used to assess stroke risk. High risk patients should be offered anticoagulation unless contra-indicated.
This scoring system has been criticised because it underestimates the effect of age as well as several other factors.

25. Stroke Risk Assessment (CHA2DS2VASc)
Alternative to CHADS2
C Chronic Heart Failure (1 point)
H Hypertension (1 point)
A Age > 75 years (2 points)
D Diabetes (1 point)
S Stroke, TIA or systemic embolisation (2 points)
V vascular disease (1 point)
A Age years (1 point)
Sc Sex category (1 point if female)
Score ≥2 = High risk – anticoagulate unless contraindicated
THE CHADSVASc scoring system has been proposed as an alternative. It adds in the effect of co-existing vascular disease and being female. It also increases the score factor associated with age.
Under this system, more patients are eligible for anticoagulation.

26. Bleeding Risk Assessment (HAS-BLED)
1 point each for:
Hypertension
Abnormal renal/liver function (1 for each)
Stroke
Bleeding history or predisposition
Labile INR
Elderly (age over 65)
Drugs*/alcohol** concomitantly (1 for each)
*Drugs that increase bleeding, e.g. aspirin
** Alcohol excess
To assess the risk of a bleed on anticoagulation, a scoring system for bleeding has been developed.
The HAS-BLED score gives an indication of how high risk a patient is. A score of >3 is considered high risk. No definitive cut-off for avoiding anticoagulation has been defined however.
It should be noted that 3 of the criteria also appear in CHADSVASc!

27. Anticoagulants Warfarin remains standard anticoagulant at present
3 new oral anticoagulants
Dabigatran (Direct thrombin inhibitor)
Licensed by MHRA
Approved by SMC
Rivaroxiban (Factor Xa inhibitor)
Apixaban (Factor Xa inhibitor)
Fixed doses
No monitoring
At least as effective as warfarin
Safer than warfarin?
Dabigatran capsules not stable outside of original blister
Very difficult to reverse effect unlike warfarin
Much more expensive (even allowing for INR costs)
Place in therapy not clear yet
Warfarin is currently the anticoagulant of choice. This is based on the experience gained over decades of use. It does however have its limitations, mainly dose variability.
Three new oral anticoagulants have been developed. All have been shown to be either:
More effective than warfarin (high dose dabigatran, apixaban)
Non-inferior to warfarin (low dose dabigatran, rivaroxaban)
As safe as warfarin (high dose dabigatran)
Safer than warfarin (low dose dabigatran, rivaroxaban, apixaban)
As of December 2011 dabigatran and rivaroxaban are licensed for AF stroke prevention. Dabigatran has also been approved by SMC with restrictions on its use agreed by the NHS. Rivaroxaban will be reviewed by SMC in February 2012
These drugs are fixed dose and do not require INR monitoring. Despite these advantages there are concerns around adherence (no monitoring, BD dosing for dabigatran and apixaban) and safety (they are not easily reversed, especially dabigatran, unlike warfarin).
They are also considerably more expensive, even allowing for the cost of warfarin monitoring.

28. Dabigatran Consensus
NHS in Healthcare Improvement Scotland Working Group:
National consensus on dabigatran
The consensus statement states that:
on balance of risks and benefits, warfarin remains the anticoagulant of clinical choice for moderate or high risk atrial fibrillation patients (CHA2DS2-VASc ≥ 2) with good INR control, and
clinicians should consider prescribing dabigatran in patients with:
poor INR control (less than 60% of time in INR range) despite evidence that they are complying, or
allergy to or intolerable side effects from coumarin anticoagulants.
The decision to use a cut-off of 60% for time in therapeutic range was based on a subgroup analysis of the RE-LY study.
The consensus document, and potential answers to frequently asked questions are available at the web address.

29. Conclusions AF is a common condition.
Patients may be unaware of its presence and are therefore at risk of a stroke
Effective treatment strategies exist to control symptoms
Effective treatment strategies exist to reduce the risk of stroke
Patient education and choice are central to improving the likelihood of treatment success

30. Tachcardia
Definition of tachycardia
Cardiac arrhythmia with a rate >100 beats per minute (bpm)

31. Types of tachycardia
Narrow complex tachycardias
Regular (supraventricular tachycardia [SVT])
Sinus tachycardia
Physiological response to insult. Impulse originates from sino-atrial (SA) node.
Atrial tachycardia
Aberrant atrial focus producing impulse independent of SA node
Atrioventricular nodal re-entry tachycardia (AVNRT)
Re-entry circuit within or near AV node

32. AV re-entry tachycardia (AVRT)
Re-entry circuit conducted from atria to ventricles via abnormal accessory pathway; usually due to Wolff-Parkinson-White (WPW) syndrome
Atrial flutter with regular AV block (eg 2:1, 3:1)
Re-entry circuit within the atria
Irregular
Atrial fibrillation (AF)
Atria twitch instead of beating in a coordinated manner

33. Broad complex tachycardias
Regular
Ventricular tachycardia (VT)
Generated by a single ventricular focus
SVT with bundle branch block (BBB)
This is rare. Any broad complex tachycardia should be treated as VT unless there the patient has an old ECG with clear previous bundle branch block of unchanged morphology.

34. Irregular
Polymorphic VT (Torsades de pointes)
Sinusoidal morphology usually due to abnormal ventricular repolarisation (long QT)
AF with bundle branch block

35. Aetiology of tachyarrhythmias (pathological as opposed to physiological)
Cardiac
Post-cardiac arrest
Post-myocardial infarction (MI)
Long QT syndrome
Valvular heart disease
Cardiomyopathy

36. Non-cardiac
Hypoxia
Hypovolaemia
Electrolyte abnormalities
Especially hypo/hyper-kalaemia, -calcaemia or -magnesaemia
Hypoglycaemia
Hypo/hyperthermia
Hypo/hyperthyroidism
Sepsis
Drug-induced
Cocaine
Amphetamines
Tricyclic antidepressants
Beta blockers
Digoxin
Amiodarone

37.  Clinical features of tachycardias
Adverse features
Shock
Hypotension, diaphoresis, pallor, increased capillary refill time (CRT)
Syncope
Transient loss of consciousness
Myocardial ischaemia
Ischaemic chest pain and/or ischaemic electrocardiogram (ECG) changes

38. Cardiac failure
Orthopnoea, paroxysmal nocturnal dyspnoea (PND), bibasal crepitations, raised jugular venous pressure (JVP)
Non-adverse features
Palpitations
Dyspnoea
Anxiety

39.  Initial investigation of tachycardia
Bloods
Full blood count
Urea & electrolytes
Magnesium
Bone profile (particularly noting calcium and phosphate)
Thyroid function tests
Other: liver function (useful pre-medication); coagulation (may need anticoagulation)
Chest radiograph (CXR)

40. Further investigation of tachycardia
Echocardiogram (echo)

41. Initial management of tachycardia
Assess patient from an ABCDE perspective
Maintain a patent airway
Use manoeuvres, adjuncts, supraglottic or definitive airways as indicated
Controlled oxygen
Maintain saturations (SpO2) 94-98%

42. Attach monitoring
Pulse oximetry
Non-invasive blood pressure
Three-lead cardiac monitoring
Defibrillator pads
12 lead ECG
Obtain intravenous (IV) access and take bloods
Give IV fluid challenge if appropriate and repeat as necessary
Identify and treat any reversible causes e.g. electrolyte abnormalities on initial VBG

43. If adverse features are present [shock, syncope, myocardial ischaemia, heart failure], prepare for emergency synchronised DC cardioversion under general anaesthesia or conscious sedation
Once ready, warn all those nearby to stand clear and remove any oxygen delivery device whilst the defibrillator is set to synchronised mode and charged to 120 J
Once the defibrillator is charged and all are clear, deliver the shock
Should this fail, two subsequent shocks at increasing increments may be tried
Should this fail, give a loading dose of amiodarone 300 mg IV over minutes and repeat DC cardioversion followed by amiodarone 900 mg IV over 24 hours

44. If adverse features are not present, assess the rhythm:
Narrow complex tachycardias (QRS duration <0.12 s)
Regular: likely SVT
Attempt vagal manoeuvres
Valsalva (ask patient to blow into syringe); carotid sinus massage.
If this fails then:
Adenosine 6 mg IV
Rapid bolus ideally into a large-bore cannula in the antecubital fossa
Warn patients of transient unpleasant side effects: flushing, nausea and chest tightness, ‘feeling of impending doom’
Avoid in patients with asthma, WPW syndrome, and denervated hearts
Caution in taking theophylline, dipyridamole or carbamazepine
If 6mg unsuccessful:

45. Adenosine 12 mg IV
If first 12mg unsuccessful:
Further adenosine 12 mg IV
If adenosine is contraindicated, consider verapamil mg IV, or flecainide 2 mg/kg IVI over min if no evidence of structural heart disease
Irregular: likely AF
Onset <48 hours

46. Aim for rhythm control
Flecainide 2 mg/kg IVI over min if no evidence of structural heart disease or amiodarone 300 mg IV over min and 900 mg over 24 hours if flecainide contraindicated
Anticoagulate with enoxaparin 1.5 mg/kg subcutaneous (SC) prior to this
Onset >48 hours
Aim for rate control
 Metoprolol 5 mg IV OR bisoprolol 5 mg orally (PO) OR verapamil 5 mg IV
If signs of heart failure try digoxin 0.5 mg IVI over min
Digoxin can be added to the above if beta-blockade unsuccessful

47. Broad complex tachycardias (QRS duration >0.12 s)
Regular
If likely monomorphic VT
Give amiodarone 300 mg IVI over min followed by amiodarone 900 mg IVI over 24 hours
Any broad complex tachycardia should be treated as VT unless there the patient has an old ECG with clear previous bundle branch block of unchanged morphology.
If definitely SVT with BBB
Try adenosine as for regular narrow complex tachycardias

48. Irregular
If likely AF with BBB
 Treat as for irregular narrow complex tachycardias
If likely polymorphic VT (Torsades de pointes)
Magnesium 2 g IV over 10 min
Stop any medications which prolong the QT interval
Correct any electrolyte abnormalities if not already done so, and give

49. Further management of tachycardia
Request 12 lead ECG once back in sinus rhythm
Look specifically for ischaemic changes (ST elevation, ST depression and T wave inversion), prolonged QT interval (QTc >440 ms) and signs of WPW syndrome (shortened PR interval, delta wave and broad QRS complex)
Identify and correct any underlying cause if not already done so
Call cardiologist
Arrange for an implantable cardioverter defibrillator (ICD) if appropriate

50. Advanced Life Support (ALS) tachycardia algorithm