Atrial Fibrillation

Atrial fibrillation can be described as a rapid, irregular, irregular atrial rhythm. The symptoms include palpitations, and occasionally insufficiency, effort intolerance, dyspnea, as well as presyncope. Atrial thrombi could develop and pose a chance of having an embolic stroke. Diagnostics are made using electrocardiography.

Treatment is based on rate control through medications and prevention of thromboembolism using anticoagulation and, sometimes, switching to sinus rhythm using the use of cardioversion or drugs.

Atrial fibrillation is attributed to multiple wavelets that have chaotic reentry into the atria. In many instances, there is an ectopic laser within the veins close to the atria (usually the pulmonary veins) that is responsible for the initiation and, possibly, the continuation the atrial fibrillation.

Atrial fibrillation occurs when the atria are not contracted as well as the atrioventricular (AV) conduction system is bombarded by a variety of electrical stimuli, leading to intermittent impulse transmission and an irregularly irregular rate of ventricular contraction that is typically in the tachycardia range.

Atrial fibrillation is one of the most prevalent arrhythmias, which affects around 2.3 million people in the US. Whites and men tend to be more susceptible to atrial fibrillation than blacks and women.

It is more prevalent with age. About 10% of all people who are over 80 years old suffer from it. Atrial fibrillation is more likely to be seen in people with underlying heart disease.

Affricillation complications

The absence of atrial contractures can lead to the formation of thromboses; annually, the probability of cerebrovascular embolic episodes is approximately 7 percent.

The risk of stroke is greater in elderly patients as well as those with a rheumatic-valvular disorder, mechanical heart valve hyperthyroidism and diabetes; hypertension, left ventricular systolic dysfunction or prior thromboembolic events.

Systemic emboli also can cause the malfunction or necrosis of other organs (eg kidneys, heart or the gastrointestinal tract, the eyes) or the body limb.

Atrial fibrillation can also impair cardiac output. The loss of atrial contractility can reduce the cardiac output at a normal heart rate by approximately 10 percent.

The decrease in cardiac output is typically accepted unless the ventricular rate gets too high (eg > 140 beats/minute) or when patients are suffering from the borderline or low cardiac output at the beginning. In such cases, heart failure may develop.

Etiology of Atrial Fibrillation

The most frequent reasons for atrial fibrillation

• Hypertension
• Coronary arterial disease
• Cardiomyopathy
• Valvular heart disorders: mitral stenosis, mitral regurgitation, tricuspid regurgitation
• Hyperthyroidism
• Binge alcohol drinking (holiday heart)

Less frequently cited reasons in atrial fibrillation are

• Embolization of the lungs
• atrial septal deformities along with other congenital heart problems
• Chronic obstructive pulmonary disorder (COPD)
• Myocarditis
• Pericarditis

Single atrial fibrillation is an atrial fibrillation that does not have any identifiable cause for patients younger than 60 years.

Classification of Atrial Fibrillation

Atrial fibrillation paroxysmal is an atrial fibrillation disorder that lasts for less than a week and has changed spontaneously or after an intervention into the normal sinus rhythm. Episodes may recur.

Persistent Atrial Fibrillation is a continuous form of atrial fibrillation that lasts for >1 week.

Atrial fibrillation that has been persistent for a long time lasts for more than one year. However, there is the possibility of getting the sinus rhythm back.

Atrial fibrillation that is permanent is not able to be converted into sinus rhythm (the term also covers patients for whom a choice was made to not try the conversion process into the sinus rhythm).

If atrial fibrillation continues to be present, the longer it remains present more likely is to undergo a spontaneous conversion and more difficult it is to convert the patient’s heart because of atrial remodelling (rapid atrial rate-induced changes to atrial electrophysiology, which are characterized by decreased atrial refractoriness and could also result in an the increase in the spatial dispersion of atrial refractoriness as well as a slowing of atrial conduction speed as well as both).

Symptoms and Signs of Atrial Fibrillation

Atrial fibrillation may be unnoticed, but a large number of patients experience palpitations, mild chest pain, or signs that indicate heart disease (eg weakening, lightheadedness, and dyspnea) in particular when the ventricular rate is extremely rapid (often 140-160 beats per minute). Patients may also show symptoms and symptoms of acute stroke, or damage to other organs caused by emboli in the system.

A pulse that is not uniformly regular, with the disappearance of the wave in the jugular venous impulse. A deficit in the pulse (the rate at which the apical ventricle is greater than the rate measured at the wrist) might be due to the fact that the left ventricular stroke volume is not always enough to generate an external pressure wave for a beat that is closely linked to the beat before it.

Diagnosis of Atrial Fibrillation

• Electrocardiography (ECG)
• Echocardiography
• Tests for thyroid function

The diagnosis of atrial fibrillation can be made through ECG (see image atrial fibrillation). The results include

• The absence of P waves
• There is a presence off (fibrillatory) waves in QRS complexes. f waves vary in their the timing and morphology, as well as in with baseline undulations of greater than 300/minute. Usually seen in lead V1 but not always visible in all leads.
• Intervals between R-R that are irregularly irregular

Atrial fibrillation

Some irregular patterns could appear similar to the atrial fibrillation pattern on ECG but are distinguished by the presence of distinct F or P waves, that can be enhanced by vagal movements.

A tremor in the muscle or electrical interference could resemble an f wave, but the actual rhythm is normal. Atrial fibrillation could also cause the appearance of ventral tachycardia or ventricular extrasystoles (Ashman condition).

This is typically the case when a short R-R period follows a long R-R period and the longer interval extends it’s refractory time of the Infra-Hisian system of conduction which is followed by a QRS complex(es) occur in an abnormal manner usually with a right bundle branch form.

Echocardiography and thyroid function tests are essential for the initial assessment. Echocardiography can be used to detect structural heart disorders (eg left atrial swelling and abnormalities in the left ventricular wall which may indicate ischemia, whether present or past and valvular conditions and cardiomyopathy) and to determine other potential risk factors of stroke (eg atrial blood stasis, the presence of thrombus or a complex aortic plaque).

Atrial thrombi tend to be found to be found in the appendages of the atrial, in which case they can be identified via transesophageal echocardiography.

Pearls & Pitfalls

• Atrial fibrillation with a wide QRS complex may indicate Wolff-Parkinson-White syndrome; in such cases, the use of AV node-blocking drugs may be fatal.

Treatment of Atrial Fibrillation

• Controlling rate with medications or ablation of AV nodes ablation
• Sometimes, rhythm control is achieved through coordinated cardioversion drugs, drugs or ablation of the substrate of atrial fibrillation.
• Prevention of the thromboembolism

If an underlying condition could be present, those suffering from new-onset atrial fibrillation could require hospitalization, however, patients who experience recurrent episodes should not require hospitalization unless additional symptoms indicate that they require it.

Once the cause has been addressed the treatment for atrial fibrillation is focused on controlling the rate of ventricular contraction as well as rhythm control and the prevention of thromboembolism.

Control of the rate of ventricular ejection

Patients suffering from atrial fibrillation of any duration need to control their rate (typically up to 100 beats/min in rest) to reduce symptoms and prevent tachycardia-induced cardiomyopathy.

For sudden paroxysms with a rapid pace (eg 140-160 beats per minute), the IV node blockers can be utilized (for doses, refer to Table Antiarrhythmic Drugs).

CAUTION: AV node blockers should not be used in patients with Wolff-Parkinson-White syndrome when an accessory AV pathway is involved (indicated by wide QRS duration); these drugs increase frequency of conduction via the bypass tract, possibly causing ventricular fibrillation.

Beta-blockers (eg, metoprolol, esmolol) are preferred if excess catecholamines are suspected (eg, in thyroid disorders, exercise-triggered cases). nondihydropyridine calcium channel blocking agents (eg, verapamil, diltiazem) are also efficient.

Digoxin is not as effective. However, it can be beneficial in cases where the heart fails is the cause. The drugs can be administered in conjunction with other medications to control the rate of heart failure for a long time. If beta-blockers and calcium channel blockers nondihydropyridine and digoxin, either in combination or separately, are not effective, amiodarone could be needed.

Pearls & Pitfalls

• AV node blockers should not be used in patients with Wolff-Parkinson-White syndrome when an accessory AV pathway is involved (indicated by wide QRS duration); these drugs increase frequency of conduction via the bypass tract, possibly causing ventricular fibrillation.

Rhythm control

In patients suffering from heart failure or hemodynamic problems directly related to atrial fibrillation that has just begun, the restoration of regular sinus rhythms is recommended to increase the cardiac output.

In other instances, the switching atrial fibrillation back to regular sinus rhythm can be ideal however, the antiarrhythmic medications that can assist in doing this (class Ia and Ic III) are at risk of adverse reactions and can cause mortality.

The conversion to sinus rhythm will not completely eliminate the need for regular anticoagulation.

To convert patients in an emergency, synchronized cardioversion or the use of drugs is an option. Before attempting conversion the ventricular rate must be controlled to less than 120 beats/minute. Also, most patients must be treated for anticoagulation (for guidelines and procedures for determining the appropriate method, refer to prevention of thromboembolism in controlling the rhythm).

If atrial fibrillation is present for longer than for 48 hours or more, the patient should be treated with the oral anticoagulant (conversion regardless of the method employed, increases the chance for thromboembolism).

Anticoagulation should be used for at least 3 weeks prior to conversion or for a shorter period prior to the conversion if the transesophageal echocardiography (TEE) is not able to detect left atrial thrombus. Anticoagulation must be maintained for at least four weeks following the cardioversion. Many patients require chronic therapy to prevent coagulation (see Long-term measures to stop bleeding thromboembolism).

Pearls & Pitfalls

• If you can, administer anticoagulation prior to trying to convert atrial fibrillation into sinus rhythm.
• Conversion to sinus rhythm will not completely eliminate the need for regular anticoagulation therapy for patients who meet the criteria for it.

A synchronized cardioversion (100 joules then 200 and 360 joules, if required) transforms atrial fibrillation into regular sinus rhythm for 75-90 percent of patients, even though the rate of recurrence is high.

The effectiveness and stability of sinus rhythm following the procedure are improved with the use of class Ia II, or III antiarrhythmic medications up to 48 hours prior to the procedure.

Cardioversion is more effective for patients who have a shorter duration of atrial fibrillation, single atrial fibrillation or atrial fibrillation due to a reversible reason but it is not as efficient for patients whose left atrium has been enlarged (greater than 5 cm) or the flow of atrial appendage is insufficient or a major underlying heart disease is evident.

The drugs that convert atrial fibrillation into sinus rhythm comprise the classes Ia (procainamide quinidine disopyramide), Ic (flecainide, propafenone) and III (amiodarone dronedarone, dofetilide Ibutilide, sotalol vernakalant) antiarrhythmics (see the table antiarrhythmic drugs). They are all effective in 50% to sixty percent of the patients however, the adverse effects vary.

They are not to be used until the rate has been reduced by a beta-blocker or a nondihydropyridine calcium channel blocker. Converting drugs that have oral formulations can also be used to maintain the sinus rate (with or without prior cardioversion). It is dependent on the tolerance of the patient.

If paroxysmal AF which occurs mostly in the evening or when vagal tone is elevated and vagolytic drugs (eg, disopyramide, for instance) could be especially beneficial. The effects of exercise-induced AF could be avoided by beta-blockers.

For certain patients with recurrent paroxysmal atrial fibrillation who also can identify its onset by symptoms, some clinicians provide a single oral loading dose of flecainide (300 mg for patients >= 70 kg, otherwise 200 mg) or propafenone (600 mg for patients >= 70 kg, otherwise 450 mg) that patients carry and self-administer when palpitations develop (“pill-in-the-pocket” approach).

This method should be restricted to patients with no sinoatrial and AV node dysfunction or bundle branch block, QT prolongation Brugada syndrome or structural heart disease. The main risk (estimated at 1percent) is the chance that it could convert atrial fibrillation into an atrial flutter with a slower rate that is a 1:1 ratio between 200 and 240 beats per minute range. The possibility of this complication could be decreased in frequency through the taking an AV suppressor drug for nodal function (eg, beta-blockers, beta-blockers, or a calcium antagonist that is not a dihydropyridine).

Angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), and aldosterone blockers may attenuate the myocardial fibrosis that provides a substrate for atrial fibrillation in patients with heart failure, but the role of these drugs in routine atrial fibrillation treatment has yet to be defined.

The prevention of thromboembolism in the control of rhythm

Patients, especially those whose current atrial fibrillation episode has been present for longer than 48 hours, face the highest risk of developing thromboembolism that lasts for several weeks following the direct or pharmacologic cardioversion.

If the time of the onset of atrial fibrillation does not occur immediately apparent within 24 hours of the event, patients need to be treated with anticoagulation for a minimum of three weeks prior to and for a minimum 4 weeks following cardioversion, regardless of the predicted probability of having a thromboembolic attack .

If therapeutic anticoagulation is begun, transesophageal ultrasound (TEE) is conducted in the event that there aren’t any left or right atrial appendage-related clots are detected, a cardioversion is performed, and then and then followed by at minimum 4 weeks of anticoagulation treatment.

In the event that urgent cardiac intervention is needed due to hemodynamic impairment The cardioversion procedure is carried out, and anticoagulation begins whenever practical and continued for a minimum of four weeks.

If the beginning of the current episode of atrial fibrillation is evident within the first 48 hours, cardioversion can be performed without anticoagulation prior to the patient suffering from non-valvular atrial fibrillation that is not at risk of risk of developing a thromboembolic condition.

Following cardioversion, therapeutic anticoagulation is administered for 4 weeks; however the anticoagulation regimen isn’t needed for patients who are at a lower risk of developing a thromboembolic condition.

After four weeks of anticoagulation therapy post-conversion Certain patients require anticoagulation for a long time ( see below) .

Ablation procedures to treat atrial fibrillation.

If patients do not respond to or do not want to utilize drugs that control rate, ablation of the AV node can be used to cause complete heart blockage; the insertion of the permanently-operated pacemaker is then needed. Ablation of just 1 AV Nodal pathway (AV modification of the node) decreases the amount of atrial impulses reaching ventricles, and also eliminates the requirement for a pacemaker. However, this method is less effective than full ablation and is not often employed.

Procedures that allow for electrically isolated veins of the pulmonary system of the left atrium could stop atrial fibrillation, but without causing an AV block. When compared to other ablation techniques, the pulmonary vein is isolated has a lower rate of success (60 to 80 percent) and more complication rates (1 to five percent).

Therefore, this procedure is typically reserved for those who are the best candidates (eg older patients who do not have significant structural heart diseases and patients with no other options like those who suffer from drug-resistant AF or with left-ventricular systolic function as well as heart failure.

Long-term prevention of the thromboembolism

Preventing thromboembolism over the long term are recommended for certain patients with atrial fibrillation the course of their risk of stroke as well as the risk of bleeding.

Patients suffering from rheumatic mitral stenosis and those with mechanical heart valves are believed to be at a high risk of developing a thromboembolic condition and so are patients with nonvalvular atrial flutter with extra risk-factors. Additional risk factors can be determined by the CHA2DS2-Vasc Score (see the table for CHA2DS2-Vasc Score).

TABLE

Guidelines for the antithrombotic treatment for atrial fibrillation are different across different regions. These currently accepted guidelines for the United States are as follows:

• Long-term anticoagulant treatment with oral anticoagulants is recommended for patients suffering from mitral stenosis due to rheumatic disease, a mechanical artificial heart valve and nonvalvular atrial fibrosis with scores of CHA2DS2-Vasc greater than 2 in males and >=3 for females (class of advice I) and is a possibility in patients with nonvalvular fibrillation and CHA2DS2-Vasc scores greater than 1 for men and greater than 2 in women (class of IIb recommendation).
• Antithrombotic therapy is not advised for patients suffering from nonvalvular atrial fibrosis and CHA2DS2-Vasc scores of 0 in males and 1 for women (class Ia of the recommendation).
• Patients suffering from atrial fibrillation and an artificial cardiac valve(s) can be treated by warfarin.
• Patients suffering from atrial fibrillation as well as significant mitral stenosis, are treated by warfarin.

In patients suffering from non-valvular atrial fibrillation that are being treated with an oral anticoagulant, A class I recommendation is provided for warfarin that has an international target normalized ratio (INR) of 2.0 to 3.0, dabigatran, Edoxaban and rivaroxaban. For patients who qualify for anticoagulant therapy using an anticoagulant that is a vitamin K antagonist such as warfarin or an anticoagulant that is not vitamin K antagonist like apixaban dabigatran or edoxaban Rivaroxaban, non-vitamin K antagonist anticoagulants are recommended (class of recommendations I).

These guidelines are modified for patients who have greater than moderate renal impairment.

Left atrial appendage could be closed surgically using a transcatheter device if the appropriate antithrombotic treatment is not recommended.

The risk for each patient’s bleeding can be assessed using one of a variety of diagnostic tools. The most popular is HAS-BLED (see the table HAS-BLED Tool to Predict Risk of Bleeding for Patients with Atrial Fibrillation). The score of HAS-BLED is most useful in finding conditions that, when modified, can reduce the risk of bleeding, as opposed to the identification of patients who have a higher risk of bleeding that are not candidates for anticoagulation.

TABLE

Key Points

• Atrial fibrillation can be described as an irregular rhythm of the atrial muscle that can be continuous or episodic Tachycardia-like paroxysms can be observed.
• QRS complexes are typically narrow; a wide complex may occur with intraventricular conduction defects or Wolff-Parkinson-White syndrome.
• Patients must undergo electrocardiography, echocardiography and thyroid function tests.
• Heart rate is usually controlled to around 100 beats per minute at rest. First-line medications include beta-blockers as well as nondihydropyridine calcium channel blocking agents (eg, verapamil, diltiazem).
• The restoration of sinus rhythm isn’t as crucial as controlling rate and does not completely eliminate the need for anticoagulation. However, it could help patients who have ongoing signs of hemodynamic dysfunction (eg, heart failure), and synchronized cardioversion drugs are available.
• Anticoagulation is typically required prior to cardioversion.
• Anticoagulation for long-term use to prevent stroke is recommended for those who are at risk of thromboembolism.