Atrial Fibrillation Revision notes
Atrial fibrillation is a common tachycardia. It is significant, as having the condition increases the risk of stroke.
Epidemiology
- Present in:
o 5% of the over 65’s
o 10% of over 70’s
o 15% of all stroke patients
§ Stroke is a major complication of AF (see below)
Causes
- Cardiac
o Heart failure
o Heart ischaemia (MI)
o Hypertension
o (Mitral) valve disease
o Congenital heart disease (rare)
- Pulmonary
o PE
o Pneumonia
o Bronchocarcinoma
- Other
o Hyperthyroidism (fast AF) –
§ Sometimes hypothyroidism can also cause slow AF
o Alcohol
o Post-operatively
o Sepsis
o High caffeine intake
o Antiarrhythmic drugs!
o ↓K+
o ↑Mg2+
- 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.
Presentation
- Often asymptomatic, but an present with:
o Palpitations
o Chest pain
o Dyspnoea
o Dizziness / syncope
- Irregularly irregular pulse – you should do an ECG on everybody with an irregular pulse!
o Apical pulse rate > radial pulse rate
o 1st heart sound of variable intensity
o Signs of LV dysfunction
Pathology
AF is an irregular atrial rhythm between 300-600bpm. The AV node is unable to transmit beats as quickly as this, and thus does so intermittently, resulting in an irregular ventricular rhythm. This irregular stimulation of the ventricles reduces cardiac output by up to 20%, as well as allowing stasis of blood in the heart chambers.
Investigations
ECG Findings
- 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
Bloods:
- U+E’s – check for renal dysfunction
- TFT’s – AF can be secondary to hyperthyroidism
- Cardiac enzymes
Echo
Can be used to look for mitral valve disease, left ventricular dysfunction, left atrial enlargement.
Management
Acute AF
This is AF <48h hours duration. patients will usually be younger and are more likely to have an identifiable cause.
- Treat the underlying condition (e.g. MI, pneumonia).
- Control the ventricular rate (see below)
- Initiate anticoagulation – 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 cerdioversion to rule out the presence of a thrombus.
- Consider mechanical or drug cardioversion (see below)
o Acutely ill patient - Mechanical cardioversion–Don’t delay treatment to give anticoagulants! Cardioversion should be perfomed 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 AF
- Control the ventricular rate
o Rate control is as good as rhythm control in chronic AF – i.e. generally you don’t need to cardiovert – as the outcomes are the same as if the rate only is well controlled. Exceptions include:Young patients, 1st episode of AF
o 1st line – β-blocker OR Ca2+ blocker
using both together is contraindicated as it can cause heart block
o 2nd line – same as above, but add digoxin, or amiodarone.
§ Digoxin as the sole treatment for AF is not widely acceptable – may be suitable for some very sedentary elderly patients.
§ Don’t give β-blockers with verapamil or diltiazem (L- type calcium channel blockers) as there is a risk of bradycardia
- Anticoagulate – with warfarin (INR 2-3) – long term therapy
o Aspirin is an inferior alternative, but may be acceptable in low risk patients (See CHADS2 score below). Usually only used if warfarin is CI’d, or in very low risk patients (CHADS ≤1)
o Check platelets and blood count, and be wary in patients with past bleeds, low Hb, high risk of falls, and on NSAID therapy.
o For more info on warfarin therapy see the Anticoagulant Therapy article
Paroxysmal AF
- 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 rhythmn. Only suitable if systolic BP >100, and no underlying LV dysfunction
o 1st line – Sotolol / bisoprolol (β-blockers)
§ Young patients – flecainide / verapamil – 1st line in younger patients, but avoided in older ones, as they are negatively ionotropic - i.e. they cause vasodilation.
o 2nd line – amiodarone – tends to be used in those with some LV dysfunction
o 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 ionotropic.
- Anticoagulate (as for chronic AF)
Cardioversion - rhythmn control
Used in two types of patient:
- Acute AF – the symptoms have been ongoing for <48h. Often amiodarone will also have been given to these patients.
- Chronic AF
o Patient has had >3 weeks of anticoagulant therapy
o TOE has proven no thrombus
o 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’
o 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.
o If the patient is on digoxin, make sure you stop the digoxin a few days before the treatment.
Mechanical cardioversion
- Should be done in an ITU or CCU setting
- Give O2
- Give sedation
- Give monophasic mechanical cardioversion, increasing the voltage if normal rhythm is not obtained:
o 100J (not commonly used, only effective in 20% of patients)
o 200J
o 360J (two attempts)
- Mechanical cardioversion has a success rate of about 70%
- The procedure
o 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 causes VF. Thus, in practice, make sure you hold down the shock button until the shock is delivered.
o Perform a full 12-lead ECG afterwards to check whether the procedure was successful.
After cardioversion continue with all the pre-cardioversion medications. Review at 3 months. Most patient who relapse do so within the first month. If still in sinus rhythm at 3 months, then you can begin to think about stopping some of the drug treatments.
Drug cardioversion
- Amiodarone is usually the drug of choice. Can be given:
o IV – 5mg/Kg in 1 hr, then a further 900mg up to 1.2g in a 24hr period
o PO –200mg/8hr for 1 week, then 200mg/12hr for 1 week, then 200mg/day maintenance.
- Flecainide is also often used, but it is negatively ionotropic (reduces the strength of contractions). Used in patients with no known IHD or WPW syndrome.
Continuing Anticoagulation
Anticoagulant therapy may be continued even if normal sinus rhythm has been restored, if other RF’s are still present. Use the CHADS2 sclae (below) to decide on the risks of continuing anti-coagulant therapy. Only discontinue anticoagulants if:
- 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)
Complications
- Stroke! – the risk of thrombo-embolic stroke, and thus the degree of anticoagulant therapy required in AF can be assessed using the CHADS2 score. All criteria are worth 1 point, except the final ‘S’. Which is worth 2 (hence the name).
o C – Cardiac Failure
o H – Hypertension
o A – Age >75
o D – Diabetes
o S – Systemic embolic event (e.g. previous stroke or TIA)
o Results:
§ Score = 0 – low risk - no specific anticoagulation
§ Score = 1 – medium risk aspirin (75mg/day) or warfarin (target INR 2-3)
§ Score ≥ 2 – high risk warfarin (target INR 2-3)
o Don’t use warfarin if contraindicated. Also be aware that warfarin itself can be a stroke risk, thus it should not be given to low risk patients.
o Warfarin reduces stroke risk by about 70% - risk in AF patients is about 4%/year. With warfarin, this is about 1%/year.
o Aspirin reduces stroke risk by about 20%
- Thrombus formation most commonly occurs in the left atrial appendage – which is very hard to view on normal 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.
Notes by Tom Leach
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