Atrial fibrillation is a common type of cardiac rhythm disturbance occurring in 1-2% of the general population and 5-15% of patients over 75 years of age. It is the most common sustained cardiac arrhythmia. Atrial fibrillation is a complex arrhythmia characterized by both abnormal automatic firing and the presence of multiple interacting re-entry circuits looping around the atria. Any conditions causing raised atrial pressure, increased atrial muscle mass, atrial fibrosis, inflammation and infiltration of the atrium can cause atrial fibrillation.
What happens during atrial fibrillation?
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| Mechanisms initiating atrial fibrillation: 1. Ectopic beats, often arising from the pulmonary veins, trigger atrial fibrillation. 2. Re-entry within the atria maintains atrial fibrillation, with multiple interacting re-entry circuits operating simultaneously. |
So basically, in atrial fibrillation, the atrial tissue depolarizes at a rate of 300-600/min. Most of these signals gets blocked at the AV node. However, the ventricles still contract at a rate of over 100/min at rest.
Source:ecgpedia.org
ECG changes in atrial fibrillation
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| ECG changes in atrial fibrillation |
- Absence of P wave.
- P wave may be replaced by fibrillatory f wave. Best seen in lead v1. f waves vary continuously in frequency, amplitude and polarity.
- R-R interval is haphazardly irregular. However, when the ventricular rate gets very fast, the R-R may appear regular and it becomes difficult to distinguish from other tachyarrhythmias such as PSVT.
- Normal shaped QRS complex because the conduction into and through the ventricles is through the normal route, that is the av node conducts in an ‘all or none’ fashion, so the depolarizing waves passing in to the bundle of his are of constant intensity. However, since the waves are irregular, the ventricles therefore contract irregularly.
- Baseline variation
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| Two examples of atrial fibrillation. The QRS complexes are irregular and there are no P waves. A: There is usually a fast ventricular rate, e.g. between 120 and 160/min, at the onset of atrial fibrillation. B: In chronic atrial fibrillation, the ventricular rate may be much slower, due to the effects of medication and AV nodal fatigue |
Classification of atrial fibrillation
Atrial fibrillation can be classified according to its nature (clinical classification) and heart rate.
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| Classification of Atrial Fibrillation |
1. Clinical classification of atrial fibrillation based on duration
| Type | Duration |
|---|---|
| First detected | Irrespective of duration or severity of symptoms |
| Paroxysmal | Atrial fibrillation that terminates spontaneously in less than 7 days. (usually less than 48 hours) |
| Persistent | Atrial fibrillation that is sustained beyond 7 days, or lasting less than 7 days but necessitating pharmacologic or electrical cardioversion |
| Long standing persistent | Continuous atrial fibrillation present for longer than 1 year |
| Permanent | Atrial fibrillation lasting for more than 1 year in a patient with a joint decision between the patient and the physician to cease further attempts to regain sinus rhythm |
2. Classification of atrial fibrillation according to heart rate
| Type | Heart Rate |
|---|---|
| Fast atrial fibrillation | Heart rate > 100/min |
| Slow atrial fibrillation | Heart rate < 100/min |
Which classification of atrial fibrillation is better?
The clinical classification is helpful in choosing between rhythm restoration and rate control. In patients with atrial fibrillation seen for the first time, it can be difficult to identify which of these is present. Atrial fibrillation may be asymptomatic and the 'first detected episode' should not be regarded as necessarily the true onset. Unfortunately for many patients, paroxysmal atrial fibrillation will become permanent as the underlying disease process that predisposes to atrial fibrillation progresses. Electrophysiological changes occur in the atria within a few hours of the onset of atrial fibrillation that tend to maintain fibrillation: electrical remodeling. When atrial fibrillation persists for a period of months, structural remodeling occurs, with atrial fibrosis and dilatation that further predispose to atrial fibrillation. Thus, early treatment of atrial fibrillation will prevent re-initiation of the arrhythmia.What is lone atrial fibrillation?
The term lone atrial fibrillation is used to describe recurrent or chronic atrial fibrillation in patients without any clinical evidence of heart disease. The parthenogenesis is unknown but genetic predisposition or even specific genetically predetermined forms of the arrhythmia have been proposed. About 30-40% of those with atrial fibrillation, especially those who present at a young age, have at least one parent with the arrhythmia, and genes associated with the sodium channel, the potassium channel, gap junction proteins and right-left isomerism have been implicated. Gene defects linked to chromosomes 10, 6, 5 and 4 have been associated with familial atrial fibrillation.
- Fifty percent patients with paroxysmal atrial fibrillation and 20% with persistent or permanent atrial fibrillation have no cause and heart is normal.
- Lone atrial fibrillation usually occurs below 60 years of age.
- It may be intermittent, later may become permanent.
- Prognosis: low risk of cerebrovascular disease (0.5% per year). Usually life span is normal.
Difference between atrial fibrillation vs atrial flutter
| Feature | Atrial fibrillation | Atrial flutter |
|---|---|---|
| Atrial wave morphology | F waves varying in shape and polarity | Identical from one f wave to another |
| Atrial wave timing | Variable: does not map out | Identical: “maps out” throughout the tracing |
| Atrial wave cycle length | Variable f-f intervals can be shorter than 180 ms (4.5 small boxes) | f-f intervals ≥ 180 ms (4.5 small boxes) |
| Ventricular (QRS) response | Completely irregular (no pattern) unless complete heart block or ventricular pacing is present | Constant (2:1, 4:1) f/r ratio or shows group beating due to patterned response (2:1-2:1-4:1) or wenckebach conduction |
| EGG findings | Appearance of fibrillation wave (f) which shows constant change in height and width. Irregularly irregular rhythm. Vibrating baseline |
Features of tachycardia. Saw-tooth appearance of T wave (flutter or F wave). Regular rhythm (irregular when there is a block). 2nd degree heart block |
One of the main differences between atrial flutter and atrial fibrillation is that atria flutter almost always occurs in the setting of structural heart disease but atrial fibrillation can develop in normal hearts. Atrial fibrillation and atrial flutter can occur in the same patient transitioning from one to the other. When atrial fibrillation converts into atrial flutter it is said that the atrial fibrillation has organized into atrial flutter. When atrial flutter converts into atrial fibrillation it is said that the atrial flutter has degenerated into atrial fibrillation. However, both are not present at the same time.
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| ECG changes in Atrial fibrillation and Atrial flutter |
Causes of atrial fibrillation
Although rheumatic heart disease, alcohol intoxication and thyrotoxicosis are the 'classic' causes of atrial fibrillation, hypertension and heart failure are the most common causes in the developed world.Paroxysmal atrial fibrillation can occur spontaneously or in healthy individuals due to excessive alcohol consumption (holiday heart syndrome). These cases usually revert to normal sinus rhythm spontaneously or are converted easily with pharmacological therapy alone.
Changes in autonomic tone in susceptible individuals may also provoke atrial fibrillation. Increased sympathetic tone due during exercise or emotional excitement, and increased vagal tone such as with sinus bradycardia during sleep may also provoke atrial fibrillation in certain susceptible individuals.
Atrial fibrillation is most frequently observed in patients with organic structural heart disease. Its prevalence rises with increasing age.
1. Common heart diseases associated with atrial fibrillation are:
- Coronary artery disease
- Hypertensive heart disease
- Valvular heart disease
Patients with coronary artery disease may sufferer from first attack of atrial fibrillation during an acute myocardial infarction or more commonly because of chronic myocardial ischemia (most probably due to associated atrial dilatation or fibrosis)
Hypertensive heart disease is often associated with left atrial enlargement.
Mitral valvular heart disease is also commonly associated with atrial fibrillation. Severe rheumatic mitral stenosis or mitral regurgitation (of any cause) produces marked left atrial enlargement which is a major predisposing factor for atrial tachyarrhythmias.
2. Other causes of atrial fibrillation include
- Thyrotoxicosis
- Cardiac surgery
- Pericardial disease (esp recurrent or chronic)
- Chronic lung disease
- Pulmonary emboli
- Cardiomyopathy
- Congenital heart disease (eg. Atrial septal disease)
- Ostructive sleep apnea
3. Common causes of atrial fibrillation
| Coronary artery disease (including acute mi) | Cardiomyopathy |
| Valvular heart disease, especially rheumatic mitral valve disease | Congenital heart disease |
| Hypertension | Chest infection |
| Sinoatrial disease | Pulmonary embolism |
| Hyperthyroidism | Pericardial disease |
| Alcohol | Idiopathic (lone atrial fibrillation) |
4. Causes of atrial fibrillation in young patients:
- Chronic rheumatic heart disease with valvular lesions, commonly mitral stenosis (ms).
- Thyrotoxicosis.
- Others: atrial septal defect (ASD), acute pericarditis, myocarditis, pneumonia.
5. Causes of atrial fibrillation in elderly patients:
- Coronary artery disease (commonly acute myocardial infarction).
- Thyrotoxicosis.
- Hypertension.
- Lone atrial fibrillation (idiopathic in 10% cases).
- Others: see above (unusual or less in chronic rheumatic heart disease).
6. Causes of temporary atrial fibrillation
- Acute myocardial infarction.
- Myocarditis (due to any cause).
- Pneumonia.
- Electrolyte imbalance.
Clinical features of atrial fibrillation
Symptoms attributable to atrial fibrillation are highly variable. In some patients (about 30%), it is an incidental finding, while others attend hospital as an emergency with rapid palpitations, dyspnea and/or chest pain following the onset of atrial fibrillation.
In patients with poor ventricular function or valve disease, it may precipitate or aggravate cardiac failure because of loss of atrial function and heart rate control. A fall in BP may cause lightheadedness, and chest pain may occur with underlying coronary artery disease.
In older patients, AF may not be associated with a rapid ventricular rate and is thus often asymptomatic, in which case it is usually discovered because of a routine examination or ECG.
The patient has an 'irregularly irregular' pulse, as opposed to a basically regular pulse with an occasional irregularity (e.g. extrasystoles) or recurring irregular patterns (e.g. Wenckebach block). The irregular nature of the pulse in atrial fibrillation is maintained during exercise.
1. Symptoms of atrial fibrillation
- Heart palpitations (feeling that your heart is racing or fluttering)
- Awareness that the heart is beating
- Chest pain, pressure, or discomfort
- Abdominal pain
- Shortness of breath
- Lightheadedness
- Fatigue or lack of energy
- Exercise intolerance
2. Signs of atrial fibrillation
- Pulse: irregularly irregular (irregular in rhythm and volume).
- BP: may be hypertensive.
- Examination of heart (heart rate to see pulsus deficit, mitral valvular or other cardiac disease).
- Thyroid status (warm sweaty hands, tremor, tachycardia, exophthalmos, thyroid gland size).
Complications of atrial fibrillation
There are two major clinical complications of atrial fibrillation:
- Systemic and pulmonary embolism (systemic from left atrium and pulmonary from right atrium). Annual risk is 5% (1 to 12%).
- Heart failure.
1. Systemic and pulmonary embolism in atrial fibrillation
Patients with atrial fibrillation have an increased risk of thromboembolism (mostly stroke). Therefore, the anticoagulation status of the patient should be reviewed and appropriate measures should be taken. Anticoagulation should not be delayed pending rate control.
The risk of stroke in atrial fibrillation depends on certain factors:
- Hypertension
- Older age (≥75)
- History of stroke symptoms or transient ischemic attack
- History of diabetes mellitus
- History of chronic heart failure
- Evidence of rheumatic heart disease
- Mechanical prosthetic heart valve
- Echocardiographic evidence of left ventricular dysfunction, left atrial enlargement or mitral annular calcification
The choice of oral anticoagulation depends on the estimated risk. It may include just aspirin (eg younger patients without other risk factors), warfarin or newer drugs such as dabigatran (a direct thrombin inhibitor). Read below in the treatment section for more information about the role and choice of anticoagulation in atrial fibrillation.
Why is there an increased risk of stroke in atrial fibrillation or atrial flutter?
Loss of atrial contraction and left atrial dilatation cause stasis of blood in the LA and may lead to thrombus formation in the left atrial appendage. This predisposes patients to stroke and other forms of systemic embolism. It usually takes at least 48 hours of arrhythmia for the thrombi to start developing.
2. Heart Failure in atrial fibrillation
The second important clinical complication of atrial fibrillation is the development of chronic heart failure.
It may occur due to:
- Decreased cardiac output from lack of atrial contraction
- Ventricular ischemia due to the rapid rate of contraction
These two events may even lead to shortness of breath and even pulmonary edema. Long term (weeks to months) continuation of rapid uncontrolled ventricular rate can lead to the development of a tachycardia-induced cardiomyopathy with ventricular dilatation and decrease in the systolic function.
Treatment of atrial fibrillation
The immediate treatment of atrial fibrillation consists of appropriate anticoagulation and rate control. Potential reversible causes and risk factors should be reviewed.
The goal of treatment of atrial fibrillation consists of:
- Rate control (A)
- Rhythm control (B)
- Treatment of primary cause
- Prevention of recurrent atrial fibrillation
- Reduction of the risk of thromboembolism (C)
(A) Rate control in atrial fibrillation
Rate control can be achieved by:
- Drugs (beta blockers, calcium channel blockers, digoxin)
- AV junctional ablation.
Rate control is usually the preferred treatment option in patients with the following:
- Permanent atrial fibrillation
- New-onset atrial fibrillation within the first 24 hours (which has about 50% chance of terminating spontaneously)
- Reversible acute illness when achievement and maintenance of sinus rhythm are unlikely until the cause is corrected (eg hyperthyroidism, metabolic abnormalities especially hypokalemia, alcohol withdrawal, acute infection)
- Asymptomatic patients who can tolerate a life-time anticoagulation
AV junctional ablation (with pacemaker implantation) can be used in patients whose rate cannot be effectively controlled with medications. It is a percutaneous procedure which electrically disconnects the atrial from the ventricles and achieves excellent rate control without further need for av nodal blocking agents. The downside is that the patient becomes pacemaker dependent. As with any of the other rate-controlling options, anti-coagulation must be continued indefinitely.
(B) Rhythm control in atrial fibrillation
Rhythm control consists of two phases:
- Sinus rhythm restoration (cardioversion)
- Sinus rhythm maintenance
1. Sinus rhythm restoration or cardioversion can be achieved by two methods:
- Chemical/Pharmacological cardioversion using anti-arrhythmic drugs
- Electrical cardioversion using direct current shock or ablation procedure
One very crucial item to review before performing any type of cardioversion is to review the patient’s anticoagulation status and thromboembolic risk because of the increase in risk of thromboembolism at the moment of transition to sinus rhythm.
Pharmacological cardioversion
Pharmacological cardioversion atrial fibrillation is of limited value as the rate of conversion to sinus rhythm is low. Intravenous ibutilide can convert up to 50% of cases of recent onset atrial fibrillation and up to 70% of atrial flutter. However, ibutilide can cause prolongation of QT interval and also torsades de pointes. Therefore, the patient needs to be carefully ECG monitored.
Direct current (electrical) cardioversion
Direct current (electrical) cardioversion (dccv) is a reliable method of restoring sinus rhythm in atrial fibrillation and atrial flutter. The shock should be synchronized with ventricular depolarization (R wave on the ECG) as otherwise unsynchronized shock can lead to ventricular fibrillation.
2. Maintenance of sinus rhythm can be achieved by antiarrhythmic drugs:
- Class I agents: flecainide, propafenone
- Class III agents: sotalol, amiodarone, dofetilide, dronedarone
Antiarrythmic drugs are modestly effective in maintaining sinus rhythm. Patients must be continuously monitored for ECG changes such as QRS interval widening (flecainide, propafenone) and QT(U) interval prolongation with the risk of torsades de pointes (sotalol, dofetilide, amiodarone, dronedarone). None of the drugs maintain sinus rhythm reliably enough to withdraw anticoagulation. Dronedarone is contraindicated in advanced heart failure.
(C) Reduction of the risk of thromboembolism
This is indicated in patients with atrial fibrillation related to rheumatic mitral stenosis or in the presence of a mechanical prosthetic heart valve. In patients with non-valvular atrial fibrillation (in the absence of mitral stenosis, artificial heart valves or mitral valve repair), a scoring system known as CHA2DS2VASc is used as the first step in determining the need for anticoagulation.
| CHA2DS2-VASc scoring system for non-valvular atrial fibrillation | ||
|---|---|---|
| Risk Factors | Score/points | |
| C | Congestive heart failure | 1 |
| H | Hypertension | 1 |
| A2 | Age ≥75 | 2 |
| D | Diabetes mellitus | 1 |
| S2 | Stroke/TIA/Thromboembolism | 2 |
| V | Vascular disease (aorta, coronary or peripheral arteries) | 1 |
| A | Age 65-74 | 1 |
| Sc | Sex category: Female | 1 |
Annual risk of stroke
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||
| Points | Risk | Treatment |
| 0 points | 0% risk | No prophylaxis required (aspirin may be given) |
| 1 point | 1.3% risk | Anticoagulant (oral) or aspirin recommended |
| 2+ points | >2.2% risk | Oral anticoagulant recommended |
Long-term prophylaxis against ischaemic stroke with oral anticoagulation must be balanced against the risk of haemorrhage. The HAS-BLED score is recommended by European, Canadian and UK (NICE) guidelines. A high HAS-BLED score identifies patients with a high risk of bleeding.
| HAS-BLED score for bleeding risk on oral anticoagulation in atrial fibrillation | |
|---|---|
| Clinical characteristic | Score/points |
| Hypertension (systolic ≥160mmHg) | 1 |
| Abnormal renal function | 1 |
| Abnormal liver function | 1 |
| Stroke in past | 1 |
| Bleeding | 1 |
| Labile INRs | 1 |
| Elderly: age ≥65 years | 1 |
| Drugs as well | 1 |
| Alcohol intake at same time | 1 |
Echocardiographic assessment (e.g. left atrial size) is of limited value in predicting stroke risk and is mainly used to identify associated structural disease. Oral anticoagulation is indicated in patients at moderate or high risk of stroke, unless there is an unacceptable bleeding risk.
Usually, warfarin is given who are at risk of stroke. Target INR following anticoagulation is 2 to 3. It reduces the risk of stroke by about two-thirds, at the cost of an annual risk of bleeding of 1–1.5%, whereas treatment with aspirin reduces the risk of stroke by only one-fifth, is associated with significant bleeding risk and, although still included in European guidelines, has a very limited role.
In lone atrial fibrillation aspirin may be given to prevent thromboembolism. In patients aged less than 65 years with no structural heart disease aspirin may be beneficial. No warfarin is given to such patients.
In intermittent AF, the risk of stroke is only loosely related to the frequency and duration of AF episodes, so stroke prevention guidelines do not distinguish between those with paroxysmal, persistent and permanent AF.
The new oral anticoagulants (NOCs) can also be used instead of warfarin. These agents fall into two classes:
- direct thrombin inhibitors (e.g. dabigatran)
- oral direct factor Xa inhibitors (e.g. rivaroxaban and apixaban)
NOACs specifically block a single step in the coagulation cascade, in contrast to warfarin, which blocks several vitamin K-dependent factors (II, VII, IX and X). Unlike warfarin, the NOACs have a rapid onset of action, shorter half-life and fewer food and drug interactions, and do not require INR testing (if warfarin is used then the target INR is 2 to 3). Trial data have shown them to be equally effective as, and safer than, warfarin. However, these agents require dose reduction or avoidance in patients with renal impairment, the elderly or those with low body weight.
For all anticoagulant drugs, comorbid conditions that may be complicated by bleeding, such as peptic ulcer, uncontrolled hypertension, alcohol misuse, frequent falls, poor drug compliance and potential drug interactions, are all relative contraindications. In warfarin-treated patients, anticoagulation can be reversed by administering vitamin K or clotting factors, but there are no current antidotes for the direct thrombin inhibitors.
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Fig: Choice of anticoagulant in atrial fibrillation: Antiplatelet therapy with
aspirin plus clopidogrel (or, less effectively, aspirin only) should be
considered in patients who refuse any oral anticoagulant therapy or cannot
tolerate anticoagulants for reasons unrelated to bleeding.
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Treatment of atrial fibrillation according to the clinical type
1. Paroxysmal atrial fibrillation:
- If asymptomatic: Does not require any treatment, follow-up the case.
- If troublesome symptoms are present: β-blocker. Other drugs such as flecainide or propafenone may be given.
- Amiodarone is effective in prevention. Low dose aspirin to prevent thromboembolism.
- If bradycardia is present (in sinoatrial disease): Permanent over drive atrial pacing (60% effective).
- In some intractable cases: Radiofrequency ablation may be required, who does not have structural heart disease (70% effective).
2. Persistent atrial fibrillation:
- Control of heart rate: β-blocker, digoxin or calcium channel blocker (verapamil, diltiazem). Combination of digoxin and atenolol may be used.
- Control of heart rhythm: DC cardioversion may be done safely. It may be repeated, if relapse occurs. Concomitant use of β-blocker or amiodarone may be used to prevent recurrence.
3. Permanent atrial fibrillation:
- Control of heart rate: Digoxin, β-blocker, calcium channel blocker (verapamil or diltiazem).
- In some cases: Transvenous radiofrequency ablation may be done (it induces complete heart block. So, permanent pacemaker should be given).
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