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Atrial fibrillation
Atrial fibrillation

Atrial fibrillation

Atrial fibrillation (AF) is an irregular, supraventricular tachycardia which has a characteristic irregularly irregular rhythm and absent P-waves on an ECG.

It is the most common sustained cardiac arrhythmia with a prevalence of 0.5% in those aged 50-59; 5% in those aged 70-75 and 10% in those aged 80-89.

Pathophysiology

The SA node is the intrinsic pacemaker of the heart, generating impulses that travel down to the AV node, depolarising the atria in the process. The AV node then passes this impulse down the bundle of His and the bundle branches before reaching the apex. It then travels up the Purkinje fibres to depolarise the rest of the ventricles.

The exact mechanisms of AF are unclear, but there are a few factors that can perpetuate the disease:

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  1. Ectopic foci - there are multiple ectopic foci (pacemakers) near the pulmonary veins in the left atrium. These are capable of rapidly firing arrhythmogenic action potentials with a typical rate of 300-600 atrial beats per minute.
  2. Abnormal atrial tissue - this perpetuates the disease. Dilated and scarred cardiac tissue in the atria sustains the arrhythmia by fractionating the action potentials into many wavelets. The more wavelets there are, the less stable the AF is.
  3. Re-entry circuits - these are propagating impulses that fail to die out and persist, thus continuously exciting the heart and shortening the refractory period.

Occasionally electrical impulses reach the AV node and the ventricles contract, but the atrial contraction rate and ventricular contraction rate are asynchronous.

With chronic AF, electrical remodelling will occur to sustain the AF. The changes are initially reversible if the sinus rhythm is restored, but may become permanent and even lead to structural changes if the fibrillation continues. This phenomenon has been termed AF begets AF.

Asynchronous firing of the atria and ventricles can lead to blood collecting and coagulating within the atrial chambers. This increases the risk of strokes as the clot could get passed into the internal carotid artery or its branches when the ventricles contract.

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āš ļø Risk factors

Cardiogenic causes of AF

  • Ischaemic heart disease - this is the most common cause in the UK.
  • Rheumatic heart disease - especially when the mitral valve is affected.
  • Hypertension
  • Pericarditis/myocarditis

Non-cardiogenic causes of AF

  • Dehydration (electrolyte imbalances)
  • Hyperthyroidism
  • Sepsis and other infections
  • Pulmonary causes - pneumonia and PE
  • Alcohol (alcohol is a diuretic and can precipitate dehydration)
  • Electrolyte imbalances - hypokalaemia, hypocalcaemia and hypomagnesaemia.

šŸ”¢ Classification

The European Society of Cardiology has 4 classifications of acute AF based on temporal factors (duration and frequency of episodes):

  1. Acute AF - this is the first detected episode in a patient who has not been diagnosed before.
  2. Paroxysmal AF - >1 episode (>30 seconds) of AF that come and go spontaneously within a period of <7 days (usually <24 hours).
  3. Persistent AF - a form of AF that is not self-terminating and lasts >7 days but may be terminated by cardioversion (drugs or electrical cardioversion) after ā‰„7 days.
    1. Long-standing persistent AF - this is a subtype of persistent AF that has had continuous AF for >1 year.
  4. Permanent AF - AF that is refractory to cardioversion and sinus rhythm cannot be restored/maintained.

šŸ˜· Presentation

  • Dyspnoea
  • Dizziness
  • Chest pain
  • Palpitations
  • Fatigue
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šŸ©ŗ
On examination:
  1. Irregularly irregular pulse
  2. Variable volume pulse
  3. Single waveform on JVP - loss of the a-wave (usually represents atrial contraction).
  4. Apical to radial pulse deficit - the radial pulses will be fewer in number compared to the number of beats heard when auscultating the apical pulse. This is because in AF, not all atrial impulses are conducted to the ventricles and subsequently the rest of the body.
  5. Variable intensity S1
Absent
Absent a-wave

šŸ” Investigations

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ECG

šŸ„‡+šŸ† It is both the first-line and gold-standard investigation that is essential to give a diagnosis of atrial fibrillation.

Itā€™s hallmark characteristics are:

  • Irregularly irregular pulse
  • Absent P-waves
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šŸ§° Management

There are 2 aspects to consider when managing AF:

  1. Rate and rhythm control
  2. Stroke prevention
ā°
Rate control:

Fast AF is when a patient has a ventricular rate >100bpm. This needs to be managed in a manner in line with all acute and emergency issues, the ABCDE approach.

  • Assess haemodynamic stability
    • Shock - suggests end-organ hypoperfusion
    • Syncope - suggests brain hypoperfusion
    • Chest pain - suggests myocardial ischaemia
    • Pulmonary oedema - suggests heart failure

      • If the patient is haemodynamically unstable ā†’ immediate DC cardioversion.

It is also important to consider reversible causes:

  1. Infection ā†’ antibiotics and fluids
  2. Dehydration ā†’ fluids
  3. Electrolyte imbalance ā†’ replenish electrolytes and correct abnormalities

šŸ’” If AF persists or reversible causes are not present then we need to think about rate or rhythm control. Until the early 2000s, the approach was to focus on rhythm control, however, nowadays the approach is predominantly focused on rate control:

Rate control should be offered to all people except those that have:

  1. Reversible cause of AF
  2. Co-existing heart failure that is primarily caused by AF
  3. New-onset AF
  4. More suitable options for rhythm control based on clinical judgement

Letā€™s take a look at our options for rate control:

šŸ„‡ First-line rate control drugs (monotherapy)

A Ɵ-blocker or rate limiting non-DHP CCB is the initial monotherapy.

  1. Ɵ-blocker - such as bisoprolol or any other Ɵ-blocker than sotalol.
    1. Contraindicated in COPD, asthma, hypotension.
  2. Rate-limiting CCB - verapamil or diltiazem (non-DHP CCB)
    1. Contraindicated in HF.

šŸ„ˆ Second-line options (dual therapy)

If monotherapy is not enough, NICE recommends a combination of 2 of the following:

  1. Ɵ-blocker - other than sotalol (this is because sotalol also has rhythm control properties).
  2. Rate-limiting CCB - verapamil or diltiazem. However, due to their negative inotropic effects they are contraindicated in HF.
  3. Digoxin - preferred with Ɵ-blocker in patients with HF or who are hypotensive.
šŸ„
Rhythm control:

Rhythm control also known as cardioversion should be offered to individuals who have:

  1. Reversible cause of AF
  2. Co-existing heart failure that is primarily caused by AF
  3. New-onset AF
  4. More suitable options for rhythm control based on clinical judgement
šŸ’”
If the patient is <65, symptomatic and has new-onset AF ā†’ cardioversion is first-line.

āš ļø It is important to remember that the moment a patient switches from AF to sinus rhythm, they have the highest risk for embolism leading to stroke. This is because the embolus is unable to leave the atria as it is fibrillating, but the moment that sinus rhythm is restored the opportunity presents itself. As such, for cardioversion to continue the patient must have had a short duration of symptoms (<48 hours) or be anticoagulated prior to cardioversion:

New-onset AF or haemodynamically unstable

šŸ„‡Ā DC cardioversion with sedation or general anaesthetic. This involves using a cardiac defibrillator machine to deliver a controlled shock in an attempt to restore sinus rhythm.

>48 hours (or uncertain onset) AF and patient is stable:

šŸ„‡Ā Anticoagulated for 3 weeks ā†’ then DC cardioversion. The patient should also be rate controlled while waiting for cardioversion (according to above guidelines).

Transoesophageal echocardiogram (TOE) to rule out embolus in the left atrial appendage before DC cardioversion.

For long-term rhythm control, we use pharmacological cardioversion:

  • šŸ„‡Ā ĆŸ-blocker - this is first-line unless there are contraindications (and not sotalol).
  • šŸ„‡Ā Flecainide - a class 1c anti-arrhythmic. It is the drug of choice for paroxysmal AF.
    • It can be given regularly or as a ā€œpill in the pocketā€ for when symptoms come on.
    • It is preferred in young patients with structurally normal hearts as it can induce fatal arrhythmias with structurally abnormal hearts.
    • Contraindications: ischaemic heart disease (IHD) and structural abnormalities.
  • šŸ„ˆĀ Amiodarone - a K+ channel blocker.
    • It is extremely effective in controlling both rate and rhythm.
    • It is the drug of choice for patients with HF and LVSD.
    • It is also used in patients with evidence of structural heart disease and new-onset AF.
    • It has a large list of severe side-effects and is typically given to older, sedentary patients.
  • šŸ„‰ Sotalol - a Ɵ-blocker and K+ channel blocker.
    • It is used in those that do not meet the demographics for either flecainide or amiodarone.

Other drugs that may be used (less commonly in the UK) include: quinidine, dofetilide, ibutilide, propafenone.

šŸ©ø
Anticoagulation in atrial fibrillation:

Embolic strokes are the main complication with AF, and therefore long-term anticoagulation is necessary.

We can stratify the risk for stroke using the CHAā‚‚-DSā‚‚-VASc score:

  • C - 1 point for congestive cardiac failure.
  • H - 1 point for hypertension.
  • Aā‚‚ - 2 points if aged >75 years old.
  • D - 1 point if the patient has diabetes mellitus.
  • Sā‚‚ - 2 points if the patient has previously had a stroke or TIA.
  • V - 1 point if the patient has known vascular disease.
  • A - 1 point if the patient is aged 65-74 years old.
  • Sc - 1 point if the patient is female (sex category)

The minimum score is 0 (0% annual stroke risk) and the maximum score is 9 (15% annual stroke risk).

Males scoring >1 or females scoring >2 require anticoagulation:

  • šŸ„‡ DOACs - such as edoxaban, apixaban, rivaroxaban, dabigatran.
    • These do not require monitoring.
    • They have less bleeding risk as compared to warfarin.
    • They have ~12 hour half-life so it is vital that doses are not missed.
  • šŸ„ˆ Warfarin
    • Requires cover with LMWH for 5 days when initiating treatment (as warfarin is initially prothrombotic).
    • Requires regular monitoring.
    • 40-hour half-life.
    • Only anticoagulant licensed for valvular AF.
  • šŸ„‰ LMWH - enoxaparin
    • This is a rare option for patients who cannot tolerate oral treatments.
    • It requires daily injections.

ā­ļø NICE guidelines advise starting anticoagulation after a stroke 2 weeks after the event (in the absence of haemorrhage) unless it is a very large cerebral infarct.

On the other end of the spectrum, anticoagulants increase the risk of bleeding. The ORBIT score can therefore be used to assess the patients bleeding risk:

The ORBIT score takes into account the following 6 factors:

  1. Sex
  2. Haemoglobin (<130 in males/<120 in females) - 2 points
  3. Age (>75 years old) - 1 point
  4. Bleeding history - 2 points
  5. Renal function (eGFR <60) - 1 point
  6. Concomitant anti-platelet use - 1 point
ORBIT score
Risk group
Bleeds per 100 patient years
0-2
Low
2.5
3
Medium
4.7
4-7
High
8.1

Atrial ablation is another option for patients who have uncontrolled symptoms with an identifiable focus in their left atrium. Patients who undergo catheter ablation still require lifelong anticoagulation as it has no benefit with regards to stroke risk.

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šŸšØ Complications

  • Heart failure
  • Systemic emboli
    • Ischaemic stroke
    • Mesenteric ischaemia
    • Acute limb ischaemia
  • Bleeding