Author: Cliff Mann / Editor: Jason Kendall / Reviewer: Martin Dore / Codes: CAP25, HAP23 / Published: 24/10/2013 / Review Date: 24/10/2016
Atrial Fibrillation affects a substantial number of patients. It thought to effect up to 3% of the population and the incidence increases with age and co-morbidities such as hypertension, heart failure, coronary artery disease, valvular heart disease, obesity, diabetes
mellitus, and chronic kidney disease. 1
The greatest morbidity and mortality associated with AF arises from the thromboembolic sequelae however significance of the dysrhythmia is highlighted by the associated odds ratios for death. In men with AF in comparison to non AF controls the Odds Ratio for death is 1.5 and in women 1.9. Most of the excess mortality occurs early after the diagnosis of AF.
The management of atrial fibrillation is seldom entirely
straightforward; the rate versus rhythm debate and the efficacy and safety of anticoagulation are just two examples of key decisions the clinician and patient must face. This situation is often compounded in patients presenting with AF to the Emergency Department as there may be uncertainty regarding onset time and relevance to the presenting complaint.
Atrial Fibrillation (AF) is an atrial tachydysrhythmia characterised by predominantly uncoordinated atrial activation with consequent deterioration of atrial mechanical function.
The p waves which represent depolarisation of the atria, are absent during atrial fibrillation and the heart rhythm is irregularly irregular.
The currently recognised classification of AF relates to the duration and persistence of the AF:
- Paroxysmal AF: AF which terminates spontaneously within seven days of onset and most often within 48 hours of onset.
- Persistent AF: AF present continuously for seven days or more or terminated by cardioversion.
- Permanent AF: AF which is accepted without attempted cardioversion or which cannot be terminated by cardioversion.2
Many of the patients who present to the Emergency Department in AF have had the condition diagnosed previously and been commenced on appropriate treatment, ie rate or rhythm control. However some will not previously been known to be in AF and will therefore require a full assessment with a view to commencing therapy.
(i) Assessment of time of rhythm onset
The most important ED determination in AF is the probable duration of the dysrhythmia. It is important as it allows the clinician to determine whether a rate or rhythm control strategy is in the best interest.
A safe time frame for cardioversion is 48 hrs from onset
Some patients present with what has often been called Fast AF. This is a misnomer since all patients in AF have chaotic atrial electrical activity with no discernible pattern, so the description fast which implies a contradistinction to slow is incorrect. The correct description is AF with a fast /slow / controlled ventricular response.
(ii) Assessment of precipitating events
There are many illnesses which may precipitate new atrial fibrillation or worsen the cardiovascular consequences of pre-existing AF.
These secondary causes can be remembered by the pneumonic
Atrial enlargement or myxoma,
Thyroid disease (check TSH and free T4 in first-time presenters),
Ethanol (Holiday heart after binging) 3
Sepsis or Sleep apnea
Where there are identifiable precipitants of atrial fibrillation they should be treated. There has been shown to be 6 fold increase in adverse event rate when treating AF secondary to an acute underlying medical illness in the emergency department. 4 The AF usually improves or resolves if treatment is directed at the precipitant.
(iii) Assessment of Haemodynamic Consequence
Most patients with AF are cardiovascularly stable. Two uncommon groups of patients may become unstable as a consequence of the onset of AF.
- Those patients in whom adequate LV function is dependent upon the 15% of ventricular filling provided by atrial contraction i.e. patients with poor LV function
- Patients in whom the ventricular response to AF results in very high heart rates (>150 bpm). In such cases there is inadequate time for LV filling with a consequent reduction in LV output and this is exacerbated by a reduction in time in diastole with a consequent reduction in coronary blood flow. This may exacerbate ischaemia and further compromise LV function.
In both groups restoration of sinus rhythm assumes increased importance and prompt cardioversion may be indicated. However for patients in the second group rate reduction may be sufficient.
Figure 2: NICE Guidance on stroke risk stratification(2)
Basic science and pathophysiology
The primary pathological change seen in atrial fibrillation is progressive atrial fibrosis. This fibrosis is usually associated with dilation of the atria and can occur as a result of a number of mechanisms including valvular and ischaemic heart disease. As a result of the dilation and fibrosis the atria undergo physical and electrical remodeling. The longer AF is present the greater and more irreversible these changes become.
In AF the normal sinus rhythm produced by regular discharges from the sino-atrial node are overwhelmed by the rapid irregularly irregular electrical discharges generated and propagated through abnormal atrial muscle. The areas most commonly implicated as the source of the dysrhythmia are the areas around the pulmonary veins.
All patients with suspected AF must undergo a physical examination, 12 lead ECG and a blood sample sent for routine haematological and biochemical analysis.
The hall-mark feature of the ECG of a patient in AF is the presence of an irregularly irregular rhythm as shown on the ECG in Figure 1.
Figure 1: 12 lead ECG of AF note irregularly irregular rhythm and lack of p waves
The differential diagnoses are atrial flutter with variable block and multifocal atrial tachycardia.
Figure 3: Atrial flutter with variable block note the characteristic saw-tooth p waves often seen best in lead V1
Figure 4: Multifocal atrial tachycardia most commonly seen in association with severe pulmonary disease.
The key features are an atrial rate in excess of 100bpm and at least 3 morphologically different non-sinus p waves in the same ECG lead
In the ED the approach to the patient in AF is determined primarily by the duration of the rhythm. In patients in whom the time of AF onset can be determined to be within 48hrs of presentation restoration of sinus rhythm is both safe and desirable. If sinus rhythm is restored patients will not require anticoagulation or further in-hospital intervention.
There is no robust evidence on which to base the choice of antidysrhythmic agent. Whilst DC cardioversion remains popular in the UK, pharmacological cardioversion with a variety of agents is established practice in many centres. Flecainide has the highest success rate with respect to restoration of sinus rhythm and is significantly quicker in onset than amiodarone. However it is recommended only in patients without evidence of ischaemic heart disease or left ventricular dysfunction. The following diagram highlights (in blue shading) the relevant sections of the algorithm published by the National Institute of Clinical Evidence(2) (see Figure 5).
Figure 5: Cardioversion Treatment Algorithm(2)
After 48hrs there is ample evidence that restoration of sinus rhythm risks dislodging thrombi from the left atrial appendage with the consequent risk of thromboembolic events including stroke.
In patients presenting after 48 hours of symptom onset or where there is doubt as to when the AF began the ED approach is limited to determining the stroke risk and controlling the ventricular rate (see Figure 6)(2). Subsequently it is necessary to decide whether the long term strategy should be one of rate or rhythm control.
Rate control, slowing the heart, increases the proportion of time and the amount of time spent in diastole thereby increasing the time available for coronary blood flow. Similarly, by increasing the time spent in diastolic filling of the ventricles, the cardiac output is increased.
Figure 6: Rate control algorithm for patients in permanent (and some persistent) AF:(2)
Rhythm control produces the same benefits via the same mechanisms but also restores atrial transport and in doing so further increases diastolic filling of the ventricles. Furthermore the maintenance of sinus rhythm reduces the problems of atrial re-modelling.
Rhythm control should be considered in all patients with persistent AF in whom there are no contra-indications. In most circumstances relevant to the ED physician this will require commencement of anticoagulation and referral to cardiology for an elective interval (6 weeks) cardioversion. During this interval it may be necessary to control the ventricular rate with a beta blocker or calcium antagonist.
Although counterintuitive, for many patients restoring sinus rhythm has not been shown to provide morbidity or mortality benefits.(3,4) In particular patients over 65 have a significantly lower all cause mortality with a rate control strategy compared with a rhythm control strategy (Evidence Class A).
A rhythm control strategy is most appropriate in the following patient groups:(3-6)
- Those who are symptomatic
- Younger patients
- Those presenting for the first time with lone atrial fibrillation
- Those with atrial fibrillation secondary to a treated / corrected precipitant
- Those with congestive heart failure.
No study has found rate control to be inferior to rhythm control (Evidence grade A)
Haemodynamically unstable AF
Rarely but importantly patients may present with haemodynamic compromise secondary to AF. Such instability due to AF rarely occurs unless the ventricular rate remains above 150 bpm for prolonged periods. It may be associated with hypotension or ischaemic chest pain. In such cases unless the AF is known to be long standing DC cardioversion is the safest and most effective treatment option(2) (See figure 7). Where the AF is longstanding the choice of agent will be governed by the presenting features. Where the main feature is ischaemic (presumably rate related) chest pain a B blocker is the most rational choice, where the main feature is hypotension a B blocker is contraindicated and therefore amiodarone would be a more rational choice.
In patients with an accessory pathway (e.g. WPW syndrome), the onset of AF may bring about profound hypotension. This occurs because the accessory pathway can conduct the fibrillation waves much more rapidly than the AV node. Nodal conduction is limited to approximately 180bpm whereas in patients with accessory pathways the rate may rise to almost 300 bpm. At such rates there is virtually no time for ventricular filling with a consequent precipitous fall in cardiac output. It is for this reason that AV nodal blocking agents should never be given to patients in AF where an accessory pathway is suspected.
Figure 7: Treatment algorithm for patients with haemodynamic instability secondary to AF(2)
Safety Issues and Pitfalls
Mis-diagnosis of Atrial Fibrillation:
- Where doubt exists a long rhythm strip is required.
- Remember the faster the rate the more regular AF will look
- AF is always irregularly irregular
- AF may co-exist with bundle branch block
- The possibility of Multi-focal atrial tachycardia and Atrial flutter should always be considered
Mis-treatment of Atrial Fibrillation:
- When a patient presents in new AF a secondary cause should be sort. Focusing on the AF alone in a patient with an acute underlying medical cause may be deleterious.
- Digoxin does not sufficiently limit AV nodal conduction when there is significant sympathetic discharge It should only be used as monotherapy in sedentary patients
- The greatest risk arising from AF is thromboembolic complications including stroke. Failure to assess and treat the stroke risk is a significant error.
- Patients with accessory pathways are at risk of sudden death if AF occurs. This risk is increased if the AV node is blocked. Therefore any patient with a known or suspected accessory pathway and an irregular rhythm should not be treated with any AV blocking agent including adenosine and B blockers
- Kirchhof P, Benussi S, Kotecha K et al. 2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS. Eur Heart J; 37: 38, 7
- NICE: Atrial Fibrillation: The management of atrial fibrillation.
- Lowenstein SR, Gabow PA, Cramer J, et al. The role of alcohol in new onset atrial fibrillation. Arch Intern Med 1983;143(10):1882-1885.
- Scheuermeyer FX. Emergency Department Patients With Atrial Fibrillation or Flutter and an Acute Underlying Medical Illness May Not Benefit From Attempts to Control Rate or Rhythm. Ann Emerg Med 2015; 65(5):511-522
- Recusitation council UK. Advances life support – Peri-arrest arrhythmias.
- Carlson J, Miketic S, Windeler J et al. randomized trial of rate-control versus rhythm-control in persistent atrial fibrillation: the Strategies of Treatment of Atrial Fibrillation (STAF) Study. J Am Coll Cardiol. 2003;41(10):1690-1696)
- Van Gelder IC, Groenveld HF, Crijns HJ, Tuininga YS, Tijssen JG, Alings AM, Hillege HL, Bergsma-Kadijk JA, Cornel JH, Kamp O, Tukkie R, Bosker HA, Van Veldhuisen DJ, Van den Berg MP, RACE II Investigators . Lenient versus strict rate control in patients with atrial fibrillation . N Engl J Med. 2010; 362: 1363 1373