Atrial fibrillation (AF) is a common tachycardia. It can be caused by many other underlying illnesses, especially in the acutely unwell patient (such as sepsis, pneumonia, hyperthyroidism or other illness) and in these instances atrial fibrillation is often reversible by treating the underlying cause.
It is also commonly found without an obvious precipitating factor, especially in older patients. These instances may present with symptoms of palpitations, or it may be discovered incidentally in the asymptomatic patient.
In the long term atrial fibrillation is significant as it increases the risk of stroke.
Managing acute atrial fibrillation is a very common problem in the emergency department with several different approaches – and is a very common exam scenario!
There are two main areas of management – managing the atrial fibrillation itself, through either rate control or rhythm control, and assessing and managing the stroke risk with anticoagulation.
Most patients who present with atrial fibrillation in the absence of an acute underlying illness can be managed appropriately in primary care. Most patients with chronic AF have a progressive disease pattern:
- Episodes of paroxysmal AF (<1 week duration)
- Often multiple episodes of this that may resolve before progressing
- Persistent AF (episodes >1 week duration)
- Long-term persistent (episodes >12 months)
- Permanent AF
Atrial fibrillation is the most common arrhythmia in adults. It is associated with an increased risk of:
- Heart Failure
- All cause mortality
Incidence increases with age.
Atrial fibrillation is present in:
- 2-4% of the general population
- 5% of the over 65’s
- 10% of over 70’s
- 15% of all stroke patients
- Stroke is a major complication of AF (see below)
- Stroke may be the first presentation of atrial fibrillation
Risk factors for AF include:
- Obstructive sleep apnoea
- Coronary artery disease
- Valvular heart disease
- Heart failure
Potentially reversible causes include:
- Alcohol excess
- Electrolyte abnormalities
Causes associated with acute presentations
- Hyperthyroidism (fast AF) –
- Sometimes hypothyroidism can also cause slow AF
- High caffeine intake
- Antiarrhythmic drugs!
Lone AF – refers to cases where no cause can be found. Many cases initially labelled as lone AF have a cause discovered upon further investigation.
Atrial fibrillation is often asymptomatic– especially in chronic AF – but acutely it can present with:
- Chest pain
- Dizziness / syncope
Irregularly irregular pulse – you should do an ECG on everybody with an irregular pulse!
- Apical pulse rate > radial pulse rate
- 1st heart sound of variable intensity
- Signs of LV dysfunction
- “Fast AF” – ventricular rate >110
- Significant symptoms
- Syncope or pre-syncope
- Chest pain
- ECG ischaemic changes
- No p waves – just an irregular baseline
- Irregular QRS – between 75-190bpm
- Normal shape QRS – because conduction through the AV node is normal
- In V1 the trace resembles atrial flutter
- Normal T waves
- U+E’s – check for renal dysfunction
- TFT’s – AF can be secondary to hyperthyroidism
- Cardiac enzymes
- CMP – calcium, magnesium and phosphate
- Many cardiologists advocate aiming for magnesium of >1 (normal range 0.7 – 1.1) in patients with AF
- Consider Holter monitor in outpatient setting
- Echocardiogram to assess for structural heart disease (transthoracic is appropriate)
- Polysomnography (sleep study) to assess for sleep apnoea – an important risk factor
There are 4 steps in the approach to managing the newly diagnosed AF patient:
- Identify risk factors and reversible causes
- Characterise any structural heart disease that may be associated with AF
- This might typically involve sending the patient for an echocardiogram
- Assess and manage ventricular rate
- Consider anticoagulation
Acute Atrial Fibrillation
- Treat the underlying condition (e.g. MI, pneumonia).
- Control the ventricular rate (see below)
- Consider anticoagulation
- See below under “Anticoagulation”
- e.g. in the acute setting with heparin (5000-10000U IV).
- This prevents thrombus formation – and thrombi are a contraindication for cardioversion. If anticoagulants are contra-indicated, then do a TOE (trans-oesophageal ultrasound) before mechanical cardioversion to rule out the presence of a thrombus.
- Consider DC or drug cardioversion (see below)
- Acutely ill patient – DC cardioversion – Don’t delay treatment to give anticoagulants! Cardioversion should be performed in an ITU setting, with sedation. The patient should be shocked at 200J initially. if this is unsuccessful, try two further attempts at 360J.
Chronic Atrial Fibrillation
Identify and treat an reversible causes
Send patient for echo to rule out any structural heart disease
Control the ventricular rate or the rhythm
- For most patients rate control is considered as effective as rhythm control in chronic AF. Exceptions include: Young patients, 1st episode of AF, significant symptoms, significant heart failure, are physically active.
- Consider a rhythm control option for those with the above exceptions
- Rate vs rhythm control shows NO difference in long-term mortality, but rhythm control does tend to result in fewer symptoms
Rate control options
- 1st line – β-blocker OR Ca2+ blocker
- using both together is contraindicated as it can cause heart block
- β-blocker is generally preferred. Atenolol, metoprolol, bisoprolol, carvedilol and nebivolol are all appropriate. Those in bold are preferred in heart failure.
- Calcium channel blockers – the appropriate calcium channel blockers are the non-dihydropyridine calcium channel blockers – diltiazem and verapamil
- 2nd line – same as above, but add digoxin, or amiodarone.
Rhythm control options
- Contraindicated if: LV dysfunction, known coronary artery disease, LV hypertrophy
- Has very long half life
- Can cause thyrotoxicosis
- Interacts with other medications
- Can cause liver impairment
- Long-term use increases risk of lung fibrosis
- Electrical cardioversion
- Most commonly used for new onset AF patients
- If known <48 hours since onset can be performed immediately – e.g. in the emergency department in a symptomatic patient with a clear time of onset
- Is also used as an elective outpatient procedure after anticoagulation
- Catheter ablation
- Most commonly use in younger patients who have failed rhythm control with other options
Assess the need for anticoagulation – see below
Assessing the need for anticoagulation
Assessing the need for anticoagulation is a very important part of managing AF. It is recommended to use the CHA2DS2-VASc (“Chads-Vasc”) score.
|C||CHF (congestive heart failure) or LVEF <40%||1|
|S2||Previous stroke, TIA or thromboembolism||2|
If using warfarin – aim for INR 2.0 – 3.0
Moderate or High
If using warfarin – aim for INR 2.0 – 3.0
Most patients with a score of 1 or more should be offered anticoagulation. But – that is not all! You must also consider the patients risk of bleeding as a result of being on anticoagulation. So, you should also consider using the HAS-BLED score to assess for the risk of bleeding. “Yes” to each item is worth 1 point. A score of ≥3 indicates a high risk of bleeding, and anticoagulation is not usually advisable, as the risks are felt to outweigh the benefits.
|H||Hypertension >160mmHg systolic|
|A||Abnormal renal or liver function|
|S||Previous history of stroke|
|B||Previous history of major bleeding|
|L||Labile INR (<60% of time in therapeutic range)|
|E||IV drug use|
|D||Drug and alcohol use – NSAIDs, anti-platelet agents, alcohol >8 weeks / week|
- NOACs don’t require monitoring of INR
- NOACs are less likely to interact with other drugs
- NOACs have standardised dosing
- BUT – NOACs are less easily reversible
- As of September 2020, a reversing agent Idarucizumab exists for Dabigatran, but not for other NOACS
- Its efficacy is somewhat controversial – it is not as straightforward as reversal of warfarin with vitamin K
- NOACs also are not recommended for use when structural heart disease is present
A note from the author – My practice when starting anticoagulants for newly diagnosed AF in the primary care setting is to start the patient on warfarin whilst we sit for an echocardiogram. This is always almost normal. I don’t think I’ve found a structural heart disease related case of AF yet in my career. Once we have the echo result a few weeks later, then I will swap the patient to a NOAC – usually rivaroxaban. Because the risk of structural heart disease appears to be so low, I know that many of my colleagues start the NOAC immediately whilst waiting for the echo.
This is a condition where short spells of AF come and go, and upon investigation, the patient may often be in sinus rhythm.
Use the ‘pill in the pocket’ treatment – i.e. flecainide or sotalol PRN – these drugs control the rhythm. Only suitable if systolic BP >100, and no underlying LV dysfunction
- 1st line – Sotolol / bisoprolol (β-blockers)
- Young patients – flecainide / verapamil – 1st line in younger patients, but avoided in older ones, as they are negatively inotropic – i.e. they cause vasodilation.
- 2nd line – amiodarone – tends to be used in those with some LV dysfunction
- 3rd line – digoxin – has a weak effect, and takes several weeks to become effective, but useful in those with severe LV dysfunction, as it is positively inotropic.
Anticoagulate (as for chronic AF)
Acute AF – the symptoms have been ongoing for <48h. Often amiodarone will also have been given to these patients.
- Patient has had >3 weeks of anticoagulant therapy
- TOE has proven no thrombus
- Unlikely if AF has been apparent for >12 months, although if it is a first attempt at cardioversion, many consultants may still ‘give it a go’
- LV dilation is a good predictor of outcome. Those with a LV of diameter >5.5cm are unlikely to have a successful cardioversion – although, again, some consultants may still try.
- If the patient is on digoxin, make sure you stop the digoxin a few days before the treatment.
- Should be done in an ITU or CCU setting
- Give O2
- Give sedation
- Give monophasic DC cardioversion, increasing the voltage if normal rhythm is not obtained:
- 100J (not commonly used, only effective in 20% of patients)
- 360J (two attempts)
- DC cardioversion has a success rate of about 70%
- The procedure
- The defibrillator needs to be in ‘sync mode’ as the shock has to be delivered at a certain point in the cycle – the R wave. If you give the shock at the T wave, you risk causing VF. Thus, in practice, make sure you hold down the shock button until the shock is delivered.
- Perform a full 12-lead ECG afterwards to check whether the procedure was successful.
Amiodarone is usually the drug of choice. Can be given:
- IV – 5mg/Kg in 1 hr, then a further 900mg up to 1.2g in a 24hr period
- PO –200mg/8hr for 1 week, then 200mg/12hr for 1 week, then 200mg/day maintenance.
Flecainide may also used, but it is negatively inotropic (reduces the strength of contractions). Used in patients with no known IHD or WPW syndrome.
- Sinus rhythm
- No RF’s for emboli (CHADS = 0)
- AF recurrence unlikely (e.g. no previous failed cardioversions, no structural heart disease, AF duration <12 months)
Stroke! – the risk of thrombo-embolic stroke, and thus the degree of anticoagulant therapy required in atrial fibrillation can be assessed using the CHA2DS2-VASc score. Any score above 2 requires anticoagulation:
|C||Congestive heart failure / LV dysfunction||1|
|S2||Stroke (previous stroke, TIA or thromboembolic disease)||2|
|V||Vascular disease (e.g. peripheral vascular disease, ischaemic heart disease, previous MI)||1|
- Score <2 – low risk – no specific anticoagulation
- Score ≥ 2 – high risk – warfarin (target INR 2-3)
- Don’t use warfarin if contraindicated. Also be aware that warfarin itself can be a stroke risk(can cause a bleed), thus it should not be given to low risk patients.
- Be wary of giving warfarin to patients at high risk of falls (typically, very old patient with many co-morbidities), s the risk from fall (and subsequent bleed) may be greater than the risk of stroke. The decision to prescribe in such instances should be taken by a senior medical practitioner and discusses with the patient and their family.
- Warfarin reduces stroke risk by about 70% – risk in AF patients is about 4% / year. With warfarin, this is about 1% / year.
- Aspirin reduces stroke risk by about 20%. Aspirin was previously recommended for low risk (score = 1 on the old CHADS2 scoring system, but this was proven to be of no benefit).
- Thrombus formation most commonly occurs in the left atrial appendage – which is very hard to view on transthoracic echo. Hence the reason why many AF patients undergo TOE – as here the echo transducer is right next to the left atrium, and can get a very good view.