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

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

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

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

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

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 300-600bpm Ventricular rate depends on degree of AV block 120-160bpm Peripheral rate slower (pulse deficit)

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

Normal Sinus Rhythm

‘Fast’ AF

‘Slow’ AF

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

Diagnosis Based on: ECG Presentation Response to treatment

Treatment objectives Rhythm / rate control Stroke prevention

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

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.

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.

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

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)

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 75-300mg warfarin to INR 2-3 See later

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

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 75-300mg Warfarin to INR 2-3 See later

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.

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 65-74 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.

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!

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.

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.

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

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

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

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

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.

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

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

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

 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

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

 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)

Further investigation of tachycardia Echocardiogram (echo)

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%

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

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 10-20 minutes and repeat DC cardioversion followed by amiodarone 900 mg IV over 24 hours

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:

Adenosine 12 mg IV If first 12mg unsuccessful: Further adenosine 12 mg IV If adenosine is contraindicated, consider verapamil 2.5-5.0 mg IV, or flecainide 2 mg/kg IVI over 20-30 min if no evidence of structural heart disease Irregular: likely AF Onset <48 hours

Aim for rhythm control Flecainide 2 mg/kg IVI over 20-30 min if no evidence of structural heart disease or amiodarone 300 mg IV over 20-30 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 30-60 min Digoxin can be added to the above if beta-blockade unsuccessful

Broad complex tachycardias (QRS duration >0.12 s) Regular If likely monomorphic VT Give amiodarone 300 mg IVI over 20-30 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

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

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

Advanced Life Support (ALS) tachycardia algorithm