Atrial Fibrillation

Atrial fibrillation (AF) is the most common cardiac dysrhythmia. It is also one of the major causes of stroke, heart failure, sudden death, and cardiovascular morbidity.

Who does AF effect?

One in four middle-aged adults in Europe and the US will develop AF and in England alone 835000 people have it.¹

Global estimates suggest an AF prevalence of approximately 3% in adults aged 20 years or older.² The prevalence of AF increases with age and with co-morbidities such as hypertension, heart failure, coronary artery disease, valvular heart disease, obesity, diabetes, mellitus, and chronic kidney disease. Due to an ageing population and an increase in conditions that predispose to AF this rate is estimated to continue to increase.

How does AF effect them?

AF can have a significant impact on quality of life. Patients can experience symptoms including lethargy, palpitations, dyspnoea, chest tightness, sleeping difficulties, and psychosocial distress.

The significance of the dysrhythmia is highlighted by the associated odds ratios for death. The odds ratio for death for those with AF compared to non-AF controls are:

• Men: 1.5:1
• Women: 1.9:1

The greatest morbidity and mortality associated with AF arises from the thromboembolic sequelae. For example, AF is thought to be an attributing factor in 20-30% of all strokes.³ Managing Stroke risk in patients with AF is therefore an essential part of the treatment strategy.

What treatment options are there?

The management of AF is seldom entirely straightforward. The rate versus rhythm debate and the efficacy and safety of anticoagulation are key decisions the clinician and patient must face.

The two most common presentations to the emergency department (ED) are:

• Acute onset AF requiring urgent/emergent management
• AF as an associated or incidental finding

The main problems are usually:

• The uncertainty regarding onset time
• The relevance to the presenting complaint

Nevertheless, there are many opportunities for the emergency physician (EP) to commence or optimise AF therapy, and thereby improve outcomes.

Learning Bite

Some patients present with what is often called fast AF. This is a misnomer since all patients in AF have chaotic atrial electrical activity with no discernible pattern. Thus, the description fast, which implies a contradistinction to slow is incorrect.

Definition

Atrial Fibrillation (AF) is an atrial tachydysrhythmia characterised by predominantly uncoordinated atrial activation with consequent deterioration of atrial mechanical function.

AF is diagnosed using an ECG which typically shows an absolutely irregular RR interval and the p waves which represent coordinated depolarisation of the atria are absent.

The currently recognised classification as per NICE 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.¹

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.

There are two main explanations thought to contribute to the prothombotic state experienced in patients with AF.

1. Structural and functional changes in the atrial myocardium along with stasis of blood especially in the Left atrial appendage allow an environment in which throbus can form.

2. Damage to the myocardium , even seen with short episodes of AF cause expression of prothrombotic factors on the atrial endothelial surface. This along with activation of platelets and inflammatory cells leads to a clot formation.¹

This can explain why even those presenting with paroxysmal AF or a brief episode should be considered for stroke risk assessment.

Investigation

All patients with suspected AF must undergo:

• A physical examination
• 12-lead ECG
• A blood sample sent for routine:
  • Haematological analysis
  • Biochemical analysis
  • Thyroid function tests

This will help tailor treatment and identify precipitants and consequences of the AF.

When a patient presents to the Emergency department in atrial fibrillation there are particular considerations in the history and physical examination that are important in deciding the most appropriate treatment.

Rhythm onset

The most important ED determination in AF is the probable onset time of the dysrhythmia as this allows the physician to decide whether rhythm or rate control is in the patients best interest.

Precipitating events

There are many illnesses which may precipitate new AF or worsen the cardiovascular consequences of pre-existing AF.

These secondary causes can be remembered by the mnemonic:

PIRATES

PE

Ischemia

Respiratory disease

Atrial enlargement or myxoma

Thyroid disease (check TSH and free T4 in first-time presenters)

Ethanol (Holiday heart after binging)⁵

Sepsis or Sleep apnea

Learning Bite

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.⁶ Careful consideration for a reversible precipitant should therefore be undertaken when assessing patients with AF in the ED. The AF usually improves or resolves if treatment is directed at the precipitant.

Haemodynamic consequence

Most patients with AF are cardiovascularly stable. However, there are two uncommon groups of patients that may become unstable as a consequence of the onset of AF:

• Patients with poor left ventricular (LV) function. Those patients in whom adequate LV function is dependent upon the 15% of ventricular filling provided by atrial contraction.
• 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. Moreover, there is a reduction of time spent in diastole with an attendant reduction in coronary blood flow. This exacerbates ischaemia and will further compromise LV function.

A patient is said to be haemodynically compromised if any of the following are present:

• Shock (BP<90 systolic)
• Loss of conciousness/syncope
• Myocardial Ischaemia (chest pain or suggestive ECG changes)
• Heart Failure
• These patients should be immediately electrically cardioverted with a synchronised DC shock.⁷

Stroke risk

The greatest morbidity and mortality associated with AF arises from the thromboembolic sequelae.

It follows that assessment and reduction of this risk is the single most important aspect of the treatment of AF.

Aims of Treatment

Fig 1 Minimising circulatory instability or insufficiency

Circulatory instability or insufficiency is normally managed by either a rhythm or rate-control strategy.

It may seem intuitive that restoring sinus rhythm would be superior to controlling the ventricular rate in the presence of AF, this is however an ongoing area of controversy. A meta-analysis by caldera et al found no benefit of rhythm control over rate control in terms of all-cause mortality, cardiovascular mortality, arrhythmic/sudden death, ischaemic stroke, systemic embolism and major bleeding.⁸

Although it is deemed safe to cardiovert patients within 48hrs of onset of AF, there has also been some concern that a significant thromboembolic risk may occur with cardioversion as early as 12 hrs from onset.⁹ Current global guidance however still stands by a 48hr window for safe cardioversion.

Many patients are very symptomatic in AF and ultimately patients should be cardioverted in the long run. Rhythm control is still therefore a mainstay of emergency department treatment.⁴ Its main benefit is appreciated in patients with acute onset AF, and patients in whom AF is thought to precede the development of heart failure and to be the primary cause of the heart failure.¹

When using a rate control strategy there is evidence to suggest lowering the ventricular rate below 110bpm does not provide any further benefit in terms of adverse clinical events. The goal therefore should be to reduce the resting ventricular rate to 110BPM or less.¹⁰

Learning Bite

If rhythm control is unsuccessful, the default option is rate control.

Stroke Risk Stratification

All patients presenting with AF, whether it be paroxysmal or persistent should be subject to a formal stroke risk assessment.

Basically, it consists of two tasks:

• Determine risk
• Consider treatment

We will consider each of these in turn.

Determine Risk

Management of Previously-identified Atrial Fibrillation

Rate Control

In patients presenting to the ED with AF with RVR who are known to have AF longterm, a reason for why they are tachycardic should be sort. If a secondary/reversible cause has been excluded then rate control should be considered.

Rate control slowing the heart increases the relative and absolute amount of time spent in diastole. This increases the time available for coronary blood flow.

Similarly, by increasing the time spent in diastolic filling of the ventricles, the cardiac output is increased.

NICE recommends rate control as the first-line strategy to people with atrial fibrillation, except in people:

• whose atrial fibrillation has a reversible cause
• who have heart failure thought to be primarily caused by atrial fibrillation
• with new-onset atrial fibrillation (<48hrs)
• for whom a rhythm control strategy would be more suitable based on clinical judgement.

Rate-control Strategy

When controlling the rate a standard B-blocker (those except sotalol) or rate limiting calcium channel blocker should be used. We will discuss specific drugs doses later in the module.

Consider digoxin only for non-paroxysmal AF for people who are sedentary or cannot use other rate-limiting options.

Management of Recent-onset, Non-Life-threatening Atrial Fibrillation

Rhythm-control Strategy

In patients in whom the onset of AF is <48 hours, the option exists to attempt to restore sinus rhythm whilst the patient is in the ED.

Rhythm control produces the same benefits through the same mechanisms as rate control but also restores atrial transport. Furthermore, the maintenance of sinus rhythm has been thought to reduce the problems of atrial re-modelling.¹²

All patients who are being considered for a rhythm control strategy should be offered anticoagulation with treatment dose LMWH (unless contraindications exist) until a full assessment has been made and further anticoagulation started. However, This should not delay emergency DCCV in the haemodynmically unstable patient.¹

Treatment

In the emergency department if patient presents within 48 hrs of onset consider either pharmacological or electrical cardioversion depending on clinical circumstances and resources.

• Electrical

Synchronised direct current (DC) cardioversion.

Unless the patient is unconscious safe sedation/GA should be undertaken as per local protocol and a starting voltage of 120-150J should be delivered, the energy can be increased in increments if this fails.⁷

• Pharmacological

Flecainide has the highest success rate with respect to restoration of sinus rhythm and is significantly quicker in onset than amiodarone, however it is contraindicated in patients with ischaemic or structural heart disease.¹³

When conducting pharmacological cardioversion in the ED:

• A choice of flecainide or amiodarone should be used in people with no evidence of structural or ischaemic heart disease.
• Amiodarone should be used in people with evidence of structural heart disease.

For patients presenting with AF of uncertain onset time or greater than 48hrs a rhythm control strategy can be implemented as an outpatient through the patients GP and through referral to a cardiology service. The patient will need at least 3 weeks of anticoagulation prior to cardioversion and the rate should be controlled in the meantime using either b-blocker or calcium channel antagonist.

An algorithm summarising the treatment of AF in the ED is shown below.

Common drugs used in the management of Atrial fibrillation

The pitfalls relating to AF can be identified into three main areas:

Misdiagnosis of AF

1. National Institute for Health and Care Excellence (NICE): Atrial fibrillation: diagnosis and management. NICE guideline [NG196] Last updated: 30 June 2021
2. Haim M, Hoshen M, et al. Prospective national study of the prevalence, incidence, management and outcome of a large contemporary cohort of patients with incident non-valvular atrial fibrillation. J Am Heart Assoc. 2015 Jan 21;4(1):e001486.
3. Kishore A, Vail A, Majid A, et al. Detection of atrial fibrillation after ischemic stroke or transient ischemic attack: a systematic review and meta-analysis. Stroke. 2014 Feb;45(2):520-6.
4. Kirchhof P, Benussi S, Kotecha D, Ahlsson A, et al. 2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS. Eur Heart J. 2016 Oct 7;37(38):2893-2962.
5. Lowenstein SR, Gabow PA, et al. The role of alcohol in new-onset atrial fibrillation. Arch Intern Med. 1983 Oct;143(10):1882-5.
6. Scheuermeyer FX, Pourvali R, Rowe BH, Grafstein E, Heslop C, MacPhee J, McGrath L, Ward J, Heilbron B, Christenson J. 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 May;65(5):511-522.e2.
7. Recusitation council UK. Advances life support Peri-arrest arrhythmias, 2021
8. Caldeira D, David C, Sampaio C. Rate versus rhythm control in atrial fibrillation and clinical outcomes: updated systematic review and meta-analysis of randomized controlled trials. Arch Cardiovasc Dis. 2012 Apr;105(4):226-38.
9. Nuotio I, Hartikainen JE, Grnberg T, Biancari F, Airaksinen KE. Time to cardioversion for acute atrial fibrillation and thromboembolic complications. JAMA. 2014 Aug 13;312(6):647-9.
10. Van Gelder IC, Groenveld HF, Crijns HJ, Tuininga YS, et al. Lenient versus strict rate control in patients with atrial fibrillation. N Engl J Med. 2010 Apr 15;362(15):1363-73.
11. Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the euro heart survey on atrial fibrillation. Chest. 2010 Feb;137(2):263-72.
12. Hagens VE, Van Veldhuisen DJ, Kamp O, et al. Effect of rate and rhythm control on left ventricular function and cardiac dimensions in patients with persistent atrial fibrillation: results from the RAte Control versus Electrical Cardioversion for Persistent Atrial Fibrillation (RACE) study. Heart Rhythm. 2005 Jan;2(1):19-24.
13. 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)