Atrial fibrillation Abhay Bajpai Edward Rowland

Atrial fibrillation (AF) is the commonest cardiac arrhythmia. The incidence increases with age and affects 5% of UK population above the age of 65 yr and 10% above 75 yr.1 2 In the United States, AF accounts for more than 35% of all admissions for cardiac arrhythmias.3 Men are 1.5 times more likely to develop AF than women. AF is often associated with structural heart disease, but in many patients it can occur with no detectable disease (lone AF). Thromboembolic events and heart failure resulting from AF lead to significant morbidity, mortality and increased cost of management.

Definition and electrocardiographic patterns AF is a supraventricular arrhythmia characterised by complete absence of coordinated atrial contractions. On the electrocardiogram there is consistent absence of P waves which are replaced by fibrillatory waves. AF is associated with an irregular and frequently rapid ventricular response if atrioventricular conduction is intact. Regular R-R intervals are possible in the presence of atrioventricular block or interference by ventricular or junctional tachycardia.3 A wide QRS complex tachycardia that is rapid, irregular or sustained strongly suggests underlying bundle branch block or conduction over an accessory pathway (e.g. Wolf–Parkinson–White syndrome) especially if the ventricular rate is extremely rapid (over 200 beats min 1). AF can be commonly associated with other arrhythmias such as atrial flutter or atrial tachycardia. Atrial flutter is a more organised and regular form of atrial activation resulting in a saw-tooth pattern or flutter waves (f) on the electrocardiogram. Atrial flutter can arise during treatment of AF with antiarrhythmic drugs. Atrial flutter itself can degenerate into AF, can be triggered by AF or the pattern can alternate between AF and flutter. Other atrial arrhythmias can also trigger AF and are identified by the presence of P waves which are separated by an isoelectric baseline.

Classification Classification of AF has always been controversial.3–5 The current classification is based on two important elements: patterns of evolution of arrhythmia and the response to treatment. First onset AF is the first clinical presentation where the patient is still in AF and the episode has been present for less than 48 h. Paroxysmal AF is the occurrence of recurrent episodes that typically last minutes to hours, occasionally days, but eventually selfterminate. Persistent AF is present when arrhythmia is not self-terminating, but pharmacological or electrical cardioversion is required to restore sinus rhythm. AF is permanent when all attempts to restore sinus rhythm have been abandoned because of physician or patient decision, frequent recurrence, or inability to cardiovert the patient.

Key points Atrial fibrillation (AF) is the commonest cardiac arrhythmia; its incidence increases with age. Diabetes mellitus, hypertension and ventricular hypertrophy are commonly associated with non-valvular atrial fibrillation. Primary aims of management of AF are conversion to sinus rhythm, maintenance of sinus rhythm and prevention of thromboembolic complications. In elderly patients who are asymptomatic, adequate rate control of AF appears to offer the same benefits as rhythm control.

Pathophysiology and mechanisms

Chronic AF carries a high risk of ischaemic stroke from thromboembolism; all patients at risk must receive adequate anticoagulation.

The mechanisms of AF are not fully clear, but at least three aspects seem to be important in its genesis and maintenance:

Anticoagulation should be continued in patients with risk factors despite successful conversion to sinus rhythm.

 There may be enhanced automaticity within ‘sleeves’ of atrial tissue that extend into the pulmonary veins or vena caval junctions.6 These foci can act as trigger points to generate multiple atrial ectopics leading to AF and their elimination by means of ablation may possibly provide a permanent cure, particularly in those with structurally normal hearts.  In chronic AF, maintenance of arrhythmia is sustained by multiple re-entering and randomly circulating wavelets that collide and divide into ‘daughter-wavelets’ thus maintaining the chaotic electrical state.7 8  The longer the duration of AF, the more difficult it is to restore sinus rhythm and prevent recurrences. This is due to electrical and structural remodelling of atrial

Abhay Bajpai Clinical Research Fellow Cardiovascular Sciences St George’s University of London London UK Edward Rowland Consultant Cardiologist St George’s Hospital London UK E-mail: [email protected] (for correspondence)

doi:10.1093/bjaceaccp/mkl051

Continuing Education in Anaesthesia, Critical Care & Pain | Volume 6 Number 6 2006 ª The Board of Management and Trustees of the British Journal of Anaesthesia [2006]. All rights reserved. For Permissions, please email: [email protected]

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Atrial fibrillation

Table 1 Causes and risk factors for AF Acute causes

AF associated with cardiovascular disease

Alcohol binge drinking Cardiac and non-cardiac surgery Myocarditis/pericarditis Pulmonary embolism Pulmonary hypertension Chest infections Hyperthyroidism

Following myocardial infarction Hypertension, especially if left ventricular hypertrophy Valvular heart disease (often mitral) Congenital heart disease, mainly atrial septal defects (ASD) Sick sinus syndrome Diabetes mellitus

Neurogenic AF

Familial AF

High vagal tone (nocturnal episodes) High sympathetic tone (daytime episodes; associated with ischaemic heart disease, stress, excessive caffeine, alcohol)

Identified in a small group of patients11

tissue resulting in shortening of effective refractory periods, thereby maintaining and increasing the duration of AF.9 10

Causes and risk factors As described above, the risk of developing AF increases with age. Whilst rheumatic valvular disease remains the most common cause for AF in developing countries, most patients develop AF on the basis of coronary artery disease and systemic hypertension. Clinically important causes and risk factors for AF are summarised in Table 1. Echocardiographic predictors include large atria, diminished ventricular function and increased left ventricular wall thickness. When AF occurs in normal hearts without signs of any demonstrable cardiovascular disease, it is termed ‘lone atrial fibrillation’

Principles of management The management of AF still represents one of the major therapeutic challenges in medicine. Based on current evidence and guidelines, there are four main principles3: (i) Restoration of sinus rhythm by pharmacological or electrical means. (ii) Control of ventricular rate during paroxysmal or persistent AF, and chronically in those with permanent AF. (iii) Prevention of recurrence of paroxysmal or persistent AF following successful restoration of sinus rhythm. (iv) Prevention of thromboembolic phenomena. When a patient is seen in the emergency setting, the main priority is to control the fast ventricular response and, depending on the haemodynamic status of patient, this can be achieved either by urgently restoring sinus rhythm or by controlling the ventricular rate. Immediate electrical cardioversion is indicated in patients with a rapid ventricular rate who are either haemodynamically unstable or have evidence of acute myocardial ischaemia or heart failure that do not respond promptly to pharmacological measures. In less acute situations, pharmacological cardioversion can be attempted, thereby avoiding the requirement for general anaesthesia.

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Cardioversion by either means carries a risk of thromboembolism, particularly when the arrhythmia has been present for longer than 48 h; anticoagulation prophylaxis must be initiated before the procedure. In the long-run, it may become appropriate to accept the arrhythmia as permanent. Recent studies have pointed out that rate controlling the AF could be at least as effective as restoration of sinus rhythm in terms of symptom control and survival, particularly in stable patients aged approximately 60 years old.

Restoration of sinus rhythm Direct current cardioversion Direct current cardioversion (DCC) involves a synchronised direct current electrical shock delivered across the chest wall. Sinus rhythm can be restored in a significant proportion of patients with success rates varying between 65% and 90%. The success of DCC appears to be greater with anterior-posterior positioning of paddles (sternum and left scapular) than with anterior-lateral (ventricular apex and right infraclavicular). Other factors include nature of heart disease, transthoracic resistance and output waveform (monophasic or biphasic).1 3 Elective DCC is performed under adequate short-acting anaesthesia. In an emergency situation, the need for anaesthesia depends on the nature of the emergency and conscious level of the patient; it is reasonable to perform DCC under conscious sedation if the urgency of the situation is such that there can be no delay. In a recent report, elective DCC performed under conscious sedation was also shown to be safe and not associated with any intolerable discomfort to the patient.12 Devices that deliver a monophasic waveform of current have been conventionally used for cardioversion. Initial shock energy of 200 J is recommended for cardioversion of AF using a monophasic device. The sequence of energy commonly used is: 200 J; 200 J; 300 J; and 360 J.3 Biphasic machines achieve cardioversion at much lower energy levels and are increasingly replacing monophasic devices. It is safe to cardiovert patients with implanted devices such as permanent pacemaker or internal defibrillator provided the implanted device is interrogated immediately before and after cardioversion to assess any malfunction. The paddles used for cardioversion should be placed as far as possible from the implanted device, preferably in the anterior-posterior position. Brief arrhythmias can arise immediately following DCC. These are mainly ventricular and supraventricular premature beats, bradycardia and short periods of sinus arrest. Ventricular tachycardia or fibrillation can be precipitated in patients with hypokalaemia and digitalis intoxication. Patients with underlying conduction defects are at risk of developing profound bradycardia, complete heart block or asystolic periods following cardioversion. These patients are identified by having a slow ventricular response to AF in the absence of rate-reducing

Continuing Education in Anaesthesia, Critical Care & Pain | Volume 6 Number 6 2006

Atrial fibrillation

medications and facilities for temporary external or endocardial pacing must be made available prior to attempting cardioversion. Electrical cardioversion can also lead to transient ST segment elevation with a rise in blood concentrations of cardiac troponins and CK-MB, even without cardiac damage. The rate of relapse after DCC is high unless anti-arrhythmic drug therapy to maintain sinus rhythm is given concomitantly. However, prophylactic therapy to prevent recurrences following DCC should be considered individually for each patient.

Pharmacological restoration of sinus rhythm Prior to considering any anti-arrhythmic therapy, it is important to realise that up to 60% of patients with recent onset AF spontaneously revert to sinus rhythm within 24 h to a few days.13 Pharmacological cardioversion is considered in patients who are haemodynamically stable; it is often successful in AF of 90%) of these triggers are now known to arise from ‘sleeves’ of atrial tissue with abnormal automaticity present within the pulmonary veins. The procedure involves isolation of pulmonary veins and radiofrequency ablation of the triggers of AF. Although the technique can provide long-term maintenance of sinus rhythm in a majority of patients, it can lead to systemic embolism and pulmonary vein stenosis, especially if multiple trigger areas are present. Methods using other energy sources, such a cryotherapy and ultrasound, are currently being evaluated and may minimise such complications.

Management in special situations Cardiac surgery The incidence of AF after cardiac surgery is high; 27–37% of patients undergoing coronary artery bypass grafting and 50% of those following valvular surgery will develop AF in the post-operative period. The majority of AF episodes occur within first 4 days of cardiac surgery with a peak incidence on the second post-operative day. Whilst it is still unclear why some patients develop AF post-operatively, certain factors have shown a statistical relationship with AF (Table 4).19 There is clear evidence that C-reactive protein, a marker of inflammation, peaks on the second post-operative day coinciding with the peak incidence of AF. This suggests a unique role of

Continuing Education in Anaesthesia, Critical Care & Pain | Volume 6 Number 6 2006

Atrial fibrillation

Table 4 Factors related to development of post-operative AF Advanced age Males Previous AF Cardiac failure Hypertension Chronic obstructive airway disease Chronic renal failure Previous cardiac surgery

Prolonged P waves on ECG Atrial dilatation High left ventricular end-diastolic pressure Cardiomegaly on chest X-ray Right coronary artery grafting Prolonged bypass time Inadequate cardioprotection and hypothermia

inflammation during the post-operative period in about 40% of patients, particularly when it involves the pericardium or the heart muscle.20 Post-operative AF is associated with increased morbidity and mortality, largely due to heart failure, stroke and prolonged hospital stay. Various therapies have been investigated for prophylaxis of post-operative AF.21 22 Guidelines3 recommend use of betablockers in patients undergoing cardiac surgery. Once a common practice to discontinue beta-blockers prior to surgery, these agents have now been shown to reduce the risk of post-operative AF by about 60%. No major differences exist between different beta-blockers (sotalol, metoprolol, propranolol) in preventing post-operative AF. Pre-operative use of amiodarone also appears to be equally effective. Haemodynamically unstable patients with AF should be cardioverted urgently, either by direct current or pharmacologically using amiodarone. Ibutilide is particularly useful in patients with atrial flutter. It is recommended that, following successful DCC, patients should receive oral amiodarone for 6–8 weeks. The vast majority of post-operative AF spontaneously reverts to sinus rhythm within 2 weeks. Thus, haemodynamically stable patients can be commenced on beta-blockers, provided these are not contraindicated, to achieve a rate control of