Atrial Fibrillation

(AF; A Fib)

Atrial fibrillation (AF) is a rapid, irregular atrial rhythm aperiodic. Symptoms include palpitations and sometimes weakness, exercise intolerance, dyspnea, and syncope. Often atrial thrombi pose a significant risk of embolic stroke form. The diagnosis results from the ECG. The therapy comprises a drug control heart rate, thromboprophylaxis with anticoagulants and in some cases, a conversion to sinus rhythm. This can be done with medication or electrical cardioversion.

Atrial fibrillation is attributed to multiple small waves with chaotic reentry mechanism within the atria. In many cases, however, is an ectopic focus within the adjacent venous structures responsible for the beginning and for the possible maintenance of the VHF (usually the pulmonary veins). In a VHF the atria do not pull together and the AV conduction system is “bombarded” with many electrical stimuli, which are responsible for a non-uniform impulse conduction and an aperiodic irregular ventricular rate, usually in tachycardia.

Atrial fibrillation (AF) is a rapid, irregular atrial rhythm aperiodic. Symptoms include palpitations and sometimes weakness, exercise intolerance, dyspnea, and syncope. Often atrial thrombi pose a significant risk of embolic stroke form. The diagnosis results from the ECG. The therapy comprises a drug control heart rate, thromboprophylaxis with anticoagulants and in some cases, a conversion to sinus rhythm. This can be done with medication or electrical cardioversion. Atrial fibrillation is attributed to multiple small waves with chaotic reentry mechanism within the atria. In many cases, however, is an ectopic focus within the adjacent venous structures responsible for the beginning and for the possible maintenance of the VHF (usually the pulmonary veins). In a VHF the atria do not pull together and the AV conduction system is “bombarded” with many electrical stimuli, which are responsible for a non-uniform impulse conduction and an aperiodic irregular ventricular rate, usually in tachycardia. The VHF is the most common arrhythmia, from the US about 2.3 million adults are affected. Fair-skinned and men are more frequently affected by VHF as Black people and women. The distribution increases with age and almost 10% of the> 80-year-olds have atrial fibrillation on. (N. D. Talk .: In Germany 0.5% of adults and 4% in the> 60-year-olds are affected.) VHF occurs primarily in patients with heart disease. Complications The lack of atrial contraction favors the formation of thrombi. On average, about 7% of patients of cerebrovascular embolic events are annually affected. The risk of stroke is higher in patients with rheumatic heart valve disease, hyperthyroidism, hypertension, diabetes mellitus, left ventricular systolic dysfunction or previous thromboembolic events. Systemic embolism can (eg. As heart, kidney, gastrointestinal tract or eyes) also cause malfunctions or necrosis of other organs or limbs. VHF can also affect cardiac output; the loss of atrial contraction can reduce cardiac output at a normal heart rate by about 10%. Such a reduction is well tolerated as a rule, unless the ventricular rate is too fast (z. B.> 140 beats / min) or in patients who have borderline or low cardiac output in advance. In such cases of heart failure may develop. Clinical Calculator: exposure to atrial fibrillation and arterial thromboembolism etiology The most common causes of atrial fibrillation are hypertension, ischiämische or not ischiämische cardiomyopathy, mitral – or Trikuspidalklappenfunktionsstörungen, hyperthyroidism and binge drinking (so-called binge drinking or holiday heart syndrome.). Among the less common causes include pulmonary embolism, atrial septal defects and other congenital cardiac malformations, COPD, myocarditis and pericarditis. A VHF unknown cause in patients <60 years is called idiopathic VHF. Classification as acute atrial fibrillation is called h with a duration of <48, a first discovered VHF. A paroxysmal atrial fibrillation is a recurrent VHF, holding usually <48 hours and spontaneously converts to normal sinus rhythm. A persistent atrial fibrillation persists> 1 week or requires a therapy for conversion to normal sinus rhythm. Long-standing persistent atrial fibrillation takes> 1 year, but it still is possible to restore sinus rhythm. A permanent atrial fibrillation can not be converted to sinus rhythm. The longer VHF continues, the less likely is a spontaneous conversion and the more difficult will cardioversion due to changes in the atria (fast, induced by the atrial rate changes in the electrophysiology of the atria, which are characterized by a decrease in the refractory of the atria and may include a slowing of conduction velocity in the atria by increasing the spatial distribution of the atrial refractory). Symptoms and complaints Atrial fibrillation is often asymptomatic. However, many patients complain of palpitations, vague chest discomfort or symptoms of heart failure (eg. as weakness, dizziness, dyspnea), v. a. at a very high frequency chamber (often 140-160 beats / min). Because systemic embolism also symptoms of acute stroke or other organ damage can show. The pulse is aperiodic irregular with a failure of the A-wave (atrial waves) in Jugularvenenpuls. A pulse deficit (frequency of the ventricular apex is higher than the groped frequency of the radial pulse) can be present as the LV stroke volume at high ventricular rates is not always sufficient to generate a blood pressure wave that is peripheral yet palpable. Diagnostic ECG echocardiography thyroid function tests The diagnosis of atrial fibrillation is done by ECG. Among the findings include the absence of P waves, F (flicker) waves between the QRS complexes (temporally irregular and different in morphology; the waveforms on the baseline at frequencies> 300 / min do not always show up in all leads ) and aperiodic irregular RR intervals (atrial fibrillation). Atrial fibrillation Other irregular rhythms can be similar in the ECG a VHF, but they are by the presence of discrete P or flutter waves that can better be visualized by vagal stimulation sometimes to distinguish them. Muscle tremors or electrical interference can resemble fibrillatory, but the underlying rhythm is regular. A VHF can also as an imitation of ventricular extrasystoles or ventricular tachycardia appear (Ashman phenomenon). This phenomenon typically appears when a long R-R interval is followed by a short. The longer interval prolongs the refractory period of the infrahisären line system, the following QRS complexes are aberrant, typically transferred to a right bundle branch block morphology. Echocardiography and thyroid function tests at the beginning of diagnostics to assess the VHF. Echocardiography provides evidence of structural heart defects (z. B. enlargement of the LA, deviations in the wall motion of the LV, suggesting a by-made or existing ischemia, valve dysfunction or cardiomyopathy) and is an important diagnostic tool for the identification of additional risk factors for stroke (z. B. Blood stasis or thrombi in the atria, complex arteriosclerotic deposits in the aorta). Thrombi in the atria can be found most likely to atrial ears; they are easier to recognize a transesophageal than transthoracic echocardiography. Tips and risks atrial fibrillation with a wide QRS complex may indicate the Wolff-Parkinson-White syndrome. In such cases, the use of AV nodal blocking drugs can be fatal. Treatment frequency control with medication or radiofrequency ablation of the AV node rhythm control of cardioversion, drugs or ablation of atrial fibrillation through a substrate thromboembolic By suspect of significant underlying dysfunction, a stationary hospitalization is recommended in patients with first Discovered VHF. In patients with recurrent AF episodes no hospital stay is required, unless other symptoms make it necessary. After an investigation of the causes, the therapy focuses on controlling the ventricular rate, rhythm and a thromboembolism. Control of ventricular patients with a VHF need (regardless of duration) frequency control (usually up to a resting rate <100 beats / min) for monitoring the symptoms and the prevention of tachykardieinduzierten cardiomyopathy. In acute paroxysmal tachycardia (z. B. 140-160 beats / min) is an i.v. Medication with AV node blockers displayed (dosages refer to the table antiarrhythmics (Vaughan-Williams classification)). Caution: AV node blockers should not be used in patients with Wolff-Parkinson-White syndrome when involved an accessory AV pathway (indicated by wide QRS complexes). AV node blockers increase the frequency of reconciliation through the bypass and may otherwise trigger ventricular fibrillation from. Beta-blockers (eg. As metoprolol, esmolol) are preferred when excess catecholamines be assumed (eg. As in diseases of the thyroid, events that are caused by movement). Calcium antagonists of the Nichtdihydropyridintyp (eg., Verapamil or diltiazem) are also effective. Digitalis is the least effective but may be the preferred drug for heart failure is present. These drugs can be administered orally at a long-term therapy for frequency control. An unsuccessful therapy with beta-blockers, calcium antagonists of the Nichtdihydropyridintyp or digitalis (administered individually or in combination) may be a treatment with amiodarone required sein.Rhythmuskontrolle In patients with heart failure or other hemodynamic disturbances directly attributable to a VHF first discovered is a restoration of normal sinus rhythm indicated for improving cardiac output. In other cases a conversion of AF to normal sinus rhythm is indeed optimal, but use the suitable antiarrhythmic agents of Class Ia, Ic and III may show side effects and increase the risk of mortality. The conversion to sinus rhythm does not constitute a waiver of a long-term anticoagulant therapy. The acute conversion is done with medication or by a synchronized cardioversion. Before attempting a conversion is made to the ventricular rate should be brought to <120 beats / min and many patients are administered an anticoagulant (see prevention of thromboembolism in rhythm control for criteria and methods). If the VHF> 48 h, an oral anticoagulant should typically be administered to the patient. (Regardless of the method of conversion is this always an increased risk of thromboembolism.) Anticoagulation should continue if possible for> 3 weeks prior to the conversion and for at least 4 weeks after cardioversion. Many patients require chronic anticoagulation, although the specific criteria are still being discussed (see Long-term measures to prevent thromboembolism). Tips and risks, if possible, run anticoagulation by before an attempt is made to convert atrial fibrillation to sinus rhythm. The conversion to sinus rhythm does not constitute a waiver of a long-term anticoagulant therapy in patients that meet the criteria. In the synchronized cardioversion (100 joules, then with 200 and 360 joules, if necessary) the VHF is converted in 75-90% of patients into a normal sinus rhythm. However, the recurrence rate is high. The effectiveness of the method and the subsequent maintenance of the sinus rhythm can be improved by the administration of antiarrhythmic agents of Class Ia, Ic or III 24-48 hours prior to cardioversion. Cardioversion is more effective in patients in whom the VHF is not so long, on the sole VHF or a VHF due to a reversible cause. It is less successful in an enlarged left atrium (> 5 cm), at a low flow rate in the atrial ears or resulting from a significant underlying heart disease. Among the drugs which are suitable for conversion of atrial fibrillation to sinus rhythm, antiarrhythmic agents of Class Ia include (procainamide, quinidine, disopyramide), Ic (flecainide, propafenone), and III (amiodarone, dofetilide, ibutilide, sotalol, see table: antiarrhythmics (Vaughan-Williams classification)). All mentioned antiarrhythmic drugs are effective in about 50-60% of patients, the side effects are different. These drugs should only be used when the rate was brought under control with a beta blocker or a calcium antagonist of the Nichtdihydropyridintyp. The drugs used for conversion are also suitable for long-term maintenance of sinus rhythm (with or without previous cardioversion). The choice of antiarrhythmic drug depends on how the patient tolerates the drug. For the treatment of paroxysmal AF that occurs exclusively or almost exclusively at rest or during sleep, d. H. if the vagal tone is increased, drugs can be particularly effective with vagolytischer effect (eg. as disopyramide). A VHF, which is triggered by exercise, might be better prevented with a beta blocker. Certain patients with recurrent paroxysmal atrial fibrillation, which can also detect by symptoms the beginning of a VHF, give some doctors a single oral dose flecainide (300 mg for patients ? 70 kg, otherwise 200 mg) or propafenone (600 mg for patients ? 70 kg, otherwise 450 mg), which carry patients and administer to himself when palpitations develop ( “pill-in-the-pocket ‘approach). This approach can be used only in patients without sinus node or AV node dysfunction, bundle branch block, QT prolongation, Brugada syndrome or structural heart disease. There is a risk (approximately 1%), that the VHF converts into a slow atrial flutter, the 1: 1 forwards in the range of 200-240 beats / min. The probability of these possible complication of the simultaneous administration of an AV node blocker (eg. As beta blockers or calcium antagonists from non-Dihydropyradin types) can be reduced. ACE-inhibitors, angiotensin II receptor antagonists, and aldosterone antagonists result in a decrease in myocardial fibrosis associated with heart failure is a substrate for a VHF in patients. The role that could play but these drugs in the routine treatment of VHF, is not yet clearly understood. Clinical Calculator: QT interval correction (ECG) prevention of thromboembolism during rhythm control patients, especially those where the current episode of AF> 48 h has been available, have a high risk of thromboembolism for several weeks after pharmacological or DC – cardioversion. If the onset of the current episode of AF is not clear within 48 hours, the patient should be anticoagulated for 3 weeks before and at least 4 weeks after cardioversion, regardless of the predicted risk of a thromboembolic event the patient (Class I recommendation). Alternatively, a therapeutic anticoagulation is started, a transesophageal echocardiography (TEE) is performed, and if no left-atrial or left atrial “appendage” blood clot is present, cardioversion can be carried out, followed by at least 4 weeks oral anticoagulation (Class IIa recommendation). When an urgent cardioversion is necessary because of hemodynamic compromise, cardioversion is performed and the anticoagulation is started as soon as possible and continued for at least 4 weeks. If the onset of the current episode of AF significantly within 48 h, cardioversion can be done without anticoagulation if the patient non-valvular AF and no high risk for thromboembolic incident has. After cardioversion therapeutic anticoagulation for 4 weeks (class I recommendation) is added; although this would not be necessary in patients with little risk of a thromboembolic event (class IIb recommendation). 4 weeks after the Post-Conversion anticoagulation need some patients, long-term anticoagulation (see below) .Ablationsverfahren for aterielle fibrillation in patients who do not respond to drug therapy for frequency control or in which it is contraindicated, an RF ablation can recommend the AV node to generate a total heart block. Then the use of a permanent pacemaker is necessary. Ablation only one AV nodal conduction path (AV node operation) reduces the number of atrial pulses are transferred to the chamber. The use of a pacemaker is unnecessary in this case, but this approach is effective as less considered a total ablation and rarely used. Ablation, in which the pulmonary veins from the left atrium are isolated, a VHF can prevent without triggering an AV block. Compared to other ablation procedures, the pulmonary vein has a lower success rate (60-80%) and a higher complication rate (1-5%). Accordingly, this method is often the best candidate subject-younger patients with drug resistant VHF that no significant structural heart disease haben.Langfristige thromboembolism The long-term measures to prevent thromboembolism are introduced for certain patients with atrial fibrillation during long-term treatment, depending on their estimated risk of stroke vs bleeding risk. Patients with rheumatic mitral stenosis and patients with mechanical heart valves are classified as patients with a high risk of a thromboembolic event, just as patients with atrial fibrillation nonvalvulärem who have additional risk factors. The additional risk factors identified by the CHADS2 score (see Table: CHADS2 Score) or CHA2DS2-VASc score (see Table: CHA2DS2-VASc score). CHADS2 score Various points (congestive) heart failure 1 Hypertension 1 Age ?75 years 1 diabetes mellitus 1 previous stroke / TIA 2 CHA2DS2-VASc score Various points (congestive) heart failure 1 Hypertension 1 Age ?75 years 2 diabetes mellitus 1 previous stroke / TIA 2 vessel disease 1 Age 65-74 years 1 sex (female) 1 The guidelines for antithrombotic therapy are fluid differ in different regions. The current guidelines in the United States are as follows:. The long-term oral anticoagulation therapy with a CHA2DS2-VASc score of ? 2 (Level I recommendation) is recommended for patients with rheumatic mitral stenosis, artificial heart valve for nonvalvuläre patients with atrial fibrillation Antithrombotic therapy is for patients with nonvalvularem atrial fibrillation and a CHA2DS2-VASc- score of 0 (level IIa recommendation) not recommended There is no antithrombotic therapy, aspirin therapy or oral anticoagulant therapy, which is recommended for patients with nichtvalvulärem atrial fibrillation and a CHA2DS2-VASc score of 1 (level IIb recommendation). Patients with atrial fibrillation and mechanical heart valve (s) are treated with warfarin. Patients with atrial fibrillation and significant mitral stenosis are treated with warfarin. In patients with AF nonvalvulärer treated with an oral anticoagulant, then a Class I indication for warfarin with a target INR of 2.0-3.0 (evidence level A), apixaban (GE B), dabigatran (evidence level B) and rivaroxaban (GE B). These general guidelines differ in patients with more than moderate renal insufficiency. The left atrial appendage can be surgically ligated or closed by means of a catheter, if appropriate antiplatelet therapy is absolutely contraindicated. The bleeding risk of the individual patient can be predicted with any number of prognostic instruments, of which the HAS-BLED most commonly used (see table: HAS-BLED score for predicting the risk of bleeding in patients with atrial fibrillation). The HAS-BLED score is most helpful to detect conditions that – if they are modified – rather the risk of bleeding reduce as patients with an increased risk of bleeding can be seen, should not receive anticoagulation. HAS-BLED score Uncontrolled for predicting the risk of bleeding in patients with atrial fibrillation Various points hypertension 1 Abnormal kidney function 1 Abnormal liver function one stroke earlier one pre-bleed 1 Labile INRs when treated with warfarin is (as a time defined in the therapeutic range with less than 60%) 1 Elderly patients (> 65 years) 1 of medication (defined as the concomitant use of an NSAID or a platelet aggregation inhibitor), 1 alcohol (defined as> 8 units of alcohol per week) 1 Clinical calculator: atrial fibrillation CHA (2) DS (2) -VASc score for clinical stroke risk calculator: HAS-BLED bleeding risk score Summary atrial fibrillation describes an aperiodic irregular atrial rhythm, which may be episodic or continuously; it may occur bouts of tachycardia. The QRS complexes should be narrow; a wide QRS complex occurs with intraventricular conduction disturbances or Wolff-Parkinson-White syndrome. It should be performed ECG and thyroid function tests. The heart rate is controlled (usually to <100 beats / min alone); First-line drugs are beta blockers and calcium channel blockers from Nichtdihydropyridintyp (eg., Verapamil, diltiazem). A restoration of sinus rhythm is less important than the frequency control. By restoring the need for anticoagulation is not superfluous, however, as patients with persistent symptoms or hemodynamic compromise (z. B. heart failure) can be helped. Here, synchronized cardioversion or drugs can be used. Anticoagulation is usually necessary before cardioversion. Long-term oral anticoagulation for stroke prevention is required for patients with risk factors for thromboembolic; Aspirin is used for those without risk factors. For more information January CT, When S, Alpert JS, et al: 2014 ACC / AHA / HRS Guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology / American Heart Association Task Force of Practice Guidelines and the Heart Rhythm Society. Circulation130: 2071-2104,, 2014.

Health Life Media Team

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