atrial fibrillation - كلية الطب · or high risk atrial fibrillation patients (cha2ds2-vasc...

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

– < 48 hours

• Paroxysmal

– variable duration

– self terminating

• Persistent

– Non-self terminating

– Cardiovertable

• Permanent

– Non-self terminating

– 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

• 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 – Rate control only

– Does not control rate during exercise

– Third choice unless others contra-indicated

Acute AF

Treatment will depend on:

• History of AF

• Time to presentation (<> 24 hours)

• Co-morbidities (CHD, CHF/LVSD etc)

• Likelihood of success (History)

• 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

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

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

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) • Licensed by MHRA

– 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

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.

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

• Anticoagulate with enoxaparin 1.5 mg/kg

subcutaneous (SC) prior to this

• 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

Advanced Life Support (ALS) Tachycardia

Algorithm