Normal the sinoatrial node produces organised electrical activity that coordinates the contraction of the atria of the heart. Atrial fibrillation is where the contraction of the atria is uncoordinated, rapid and irregularly. This due to disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node. An ECG will show an absence of p waves. This reflects the lack of coordinated atrial electrical activity. This disorganised electrical activity in the atria also leads to irregular conduction of electrical impulses to the ventricles. This results in:
- Irregularly irregular ventricular contractions
- Heart failure due to poor filling of the ventricles during diastole
- Risk of stroke
There is a tendency for blood to collect in the atria and form blood clots. These clots can become emboli, travel to the brain and block the cerebral arteries causing an ischaemic stroke.
Patients are often asymptomatic and incidentally picked up when attending for other reasons.
Presenting symptoms can be:
- Shortness of breath
- Syncope (dizziness or fainting)
- Symptoms of associated conditions (e.g. stroke, sepsis or thyrotoxicosis)
Irregularly irregular pulse
There are two differential diagnoses for an irregularly irregular pulse:
- Atrial fibrillation
- Ventricular ectopics
These can be differentiated using an ECG. An ECG should be performed on everyone with an irregularly irregular pulse.
Ventricular ectopics disappear when the heart rate gets over a certain threshold. Therefore a regular heart rate during exercise suggests a diagnosis of ventricular ectopics.
AF on an ECG
- Absent P waves
- Narrow QRS Complex Tachycardia
- Irregularly irregular ventricular rhythm
Valvular Versus Non-Valvular AF
Valvular AF is defined as patients with AF who also have moderate or severe mitral stenosis or a mechanical heart valve. The assumption is that the valvular pathology itself has lead to the atrial fibrillation. AF without valve pathology or with other valve pathology such as mitral regurgitation or aortic stenosis is classed as non-valvular AF.
Most common causes of AF (remember that AF affects mrs SMITH)
- Mitral Valve Pathology (stenosis or regurgitation)
- Ischemic Heart Disease
Principles of treating AF
This is based on the most recent NICE guidelines from 2014 and has been adapted to make it easy to learn. Please read the full guideline before putting it into practice on real patients.
There are two principles to treating atrial fibrillation:
- Rate or rhythm control
- Anticoagulation to prevent stroke
Rate Control (vs rhythm control)
Normally the function of the atria is to pump blood in to the ventricles. In AF atrial contractions are not coordinated so the ventricles have to fill up by suction and gravity. This is considerably less efficient. The higher the heart rate, the less time is available for the ventricles to fill with blood, reducing the cardiac output. The aim is to get the heart rate below 100 to extend the time during diastole when the ventricles can fill with blood.
NICE guidelines (2014) suggest all patients with AF should have rate control as first line unless:
- There is reversible cause for their AF
- Their AF is of new onset (within the last 48 hours)
- Their AF is causing heart failure
- They remain symptomatic despite being effectively rate controlled
Options for Rate Control:
- Beta blocker is first line (e.g. atenolol 50-100mg once daily)
- Calcium-channel blocker (e.g. diltiazem) (not preferable in heart failure)
- Digoxin (only in sedentary people, needs monitoring and risk of toxicity)
Rhythm control can be offered to patients where:
- There is a reversible cause for their AF
- Their AF is of new onset (<48 hours)
- Their AF is causing heart failure
- They remain symptomatic despite being effectively rate controlled
The aim of rhythm control is to return the patient to normal sinus rhythm. This can be achieved through a single “cardioversion” event that puts the patient back in to sinus rhythm or long term medical rhythm control that sustains a normal rhythm.
Consider cardioversion in a candidate for rhythm control. There is a choice between immediate cardioversion or delayed cardioversion:
- Immediate cardioversion if the AF has been present for less than 48 hours or they are severely haemodynamically unstable.
- Delayed cardioversion if the AF has been present for more than 48 hours and they are stable.
In delayed cardioversion the patient should be anticoagulated (see below) for a minimum of 3 weeks prior to cardioversion. Anticoagulation is essential because during the 48 hours prior to cardioversion they may have developed a blood clot in the atria and reverting them back to sinus rhythm carries a high risk of mobilising that clot and causing a stroke. They should have rate control whilst waiting for cardioversion.
There are two options for cardioversion:
- Pharmacological cardioversion
- Electrical cardioversion
NICE guidelines (2014) say for pharmacological cardioversion first line is:
- Amiodarone (the drug of choice in patients with structural heart disease)
The aim of electrical cardioversion is to rapidly shock the heart back into sinus rhythm. This involves sedation or a general anaesthetic and using a cardiac defibrillator machine to deliver controlled shocks in an attempt to restore sinus rhythm.
Long Term Medical Rhythm Control:
- Beta blockers are first line for rhythm control
- Dronedarone is second line for maintaining normal rhythm where patients have had successful cardioversion
- Amiodarone is useful in patients with heart failure or left ventricular dysfunction
Paroxysmal Atrial Fibrillation
Paroxysmal AF is when the AF comes and goes in episodes, usually not lasting more than 48 hours. Patients should still be anti coagulated based on CHADSVASc score. They may be appropriate for a “pill in the pocket” approach. This is where they take a pill to terminate their atrial fibrillation only when they feel the symptoms of AF starting. To be appropriate for a pill in the pocket approach they need to have infrequent episodes without any underlying structural heart disease. They also need to be able to identify when they are in AF and understand when the treatment is appropriate.
Flecanide is the usual treatment for a “pill in the pocket” approach.
N.B. Avoid flecanide in atrial flutter as it can cause 1:1 AV conduction and resulting in a significant tachycardia.
The uncontrolled and unorganised movement of the atria leads to blood stagnating in the left atrium, particularly in the atrial appendage. Eventually this stagnated blood leads to a thrombus (clot). This clot then mobilises (becomes an embolus) and travels with the blood. It travels from the atria, to the ventricle, to the aorta then up in the carotid arteries to the brain. It can then lodge in the cerebral arteries and cause an ischaemic stroke.
Anticoagulation acts to prevent coagulation (thrombus formation) by interfering with the clotting cascade. For perspective:
- WITHOUT anticoagulation, patients with AF have around a 5% risk of stroke each year (depending on CHADSVASc score).
- WITH anticoagulation, patients with AF have around a 1-2% risk of stroke each year (depending on CHADSVASc score). Anticoagulation reduces the risk of stroke by about 2/3.
Patients on anticoagulation have around a 3% risk of having a serious bleed each year depending on their HAS-BLED score. Generally bleeds are more reversible than strokes and have less long term consequences.
Warfarin is a vitamin K antagonist. Vitamin K is essential for the functioning of several clotting factors and warfarin blocks vitamin K. It prolongs the prothrombin time, which is the time it takes for blood to clot.
We measure INR (international normalised ratio), to assess how anticoagulated the patient is by warfarin. The INR is a calculation of how the prothrombin time of the patient compares with the prothrombin time of a normal health adult. An INR of 1 indicates a normal prothrombin time. An INR of 2 indicates that the patient has a prothrombin time twice that of a normal healthy adult (it takes them twice as long to form a blood clot).
Being started on warfarin is a reasonably large undertaking. It requires close monitoring of their INR and frequent dose adjustments to keep the INR in range. It is given once a day and usually at 6pm in hospital so that INR can be obtained prior to dose. The target INR for AF is 2 – 3.
Warfarin is affected by the cytochrome P450 system in the liver. This system is involved in the metabolism of warfarin. The INR will be affected by other drugs that influence the activity of the P450 system. This includes many antibiotics.
INR is also affected by many foods such those that contain vitamin K such as leafy green vegetables and those that affect P450 such as cranberry juice and alcohol. This means it is important to monitor INR more closely when the patient changes medications or their diet.
Warfarin has a half-life of 1-3 days. It is also reversible with vitamin K in the event that the INR is very high or bleeding has occurred.
NOvel AntiCoagulants (NOACS) (i.e. apixaban, dabigatran, rivaroxaban)
NOACS are now often referred to as Direct acting Oral AntiCoagulants (DOACS). They are currently on patent, which means the drugs companies that produce them can charge more money for them. For example it costs £27 for apixaban versus £1 for warfarin per month. This is often offset by the cost of monitoring warfarin and they will soon be coming off patent at which point they will become much cheaper (in the year 2022 for apixaban).
Apixaban and dabigatran are taken twice daily, rivaroxaban is taken once daily. NOACs have a 7-15 hour half-life, so reverse themselves in a short space of time. Apixaban has a half-life of approximately 12 hours.
When there is uncontrolled or life-threatening bleeding, the anticoagulant effects can be reversed using:
- Andexanet alfa (apixaban and rivaroxaban)
- Idarucizumab (a monoclonal antibody against dabigatran)
DOACS have a number of advantages compared with warfarin (BMJ, 2017):
- No monitoring is required
- No major interaction problems
- Equal or slightly better than warfarin at preventing strokes in AF
- Equal or slightly less risk of bleeding than warfarin
This is a tool for assessing whether a patient with atrial fibrillation should be started on anticoagulation. It is essentially a list of risk factors, and if you have one or more of these risk factors then anticoagulation should be considered or started. The higher the score the higher the risk of developing a stroke or TIA and the greater the benefit from anticoagulation.
There is no role for aspirin in preventing stroke in AF. This used to be recommended, but not any longer.
- 0: no anticoagulation
- 1: consider anticoagulation
- >1: offer anticoagulation
- C – Congestive heart failure
- H – Hypertension
- A2 – Age >75 (Scores 2)
- D – Diabetes
- S2 – Stroke or TIA previously (Scores 2)
- V – Vascular disease
- A – Age 65-74
- S – Sex (female)
HAS-BLED is an assessment tool for establishing a patient’s risk of major bleeding whilst on anticoagulation. It can be used prior to initiating anticoagulation or as a monitoring tool in patients with a high risk of bleeding. It is not as essential to know inside out as the CHADSVASc but is useful to be aware of if you think a patient might have a higher risk of bleeding (for example those with at risk of falls). It is useful in practice for comparing the risk of stroke to the risk of bleeding to help patients and doctors make an informed decision about whether to start anticoagulation or not. Usually the risk of stroke significantly outweighs the risk of bleeding. Also, most bleeding can be treated, whereas a stroke often leads to significant long term morbidity and a lower quality of life.
The easiest way to calculate the HAS-BLED score is with an online calculator that will provide a risk of bleeding based on their score. It is scored based on:
- H – Hypertension
- A – Abnormal renal and liver function
- S – Stroke
- B – Bleeding
- L – Labile INRs (whilst on warfarin)
- E – Elderly
- D – Drugs or alcohol
Last updated November 2018