The pulse is irregularly irregular with loss of a waves in the jugular venous pulse. A pulse deficit the apical ventricular rate is faster than the rate palpated at the wrist may be present because left ventricular stroke volume is not always sufficient to produce a peripheral pressure wave for a beat closely coupled to the previous beat. Diagnosis of atrial fibrillation is by ECG see figure Atrial fibrillation Atrial fibrillation Atrial fibrillation is a rapid, irregularly irregular atrial rhythm.
Atrial thrombi may form Findings include. Other irregular rhythms may resemble atrial fibrillation on ECG but can be distinguished by the presence of discrete P or flutter waves, which can sometimes be made more visible with vagal maneuvers. Muscle tremor or electrical interference may resemble f waves, but the underlying rhythm is regular. Atrial fibrillation may also cause a phenomenon that mimics ventricular extrasystoles or ventricular tachycardia Ashman phenomenon.
This phenomenon typically occurs when a short R-R interval follows a long R-R interval; the longer interval lengthens the refractory period of the infra-Hisian conduction system, and the subsequent QRS complex es are conducted aberrantly, typically with right bundle branch morphology.
Echocardiography Echocardiography This photo shows a patient having echocardiography. This image shows all 4 cardiac chambers and the tricupsid and mitral valves.
Echocardiography uses ultrasound waves to produce an image of Follicular cells in the gland produce the 2 main thyroid hormones Echocardiography is done to assess structural heart defects eg, left atrial enlargement, left ventricular wall motion abnormalities suggesting past or present ischemia, valvular disorders, cardiomyopathy and to identify additional risk factors for stroke eg, atrial blood stasis or thrombus, complex aortic plaque.
Atrial thrombi are more likely in the atrial appendages, where they are best detected by transesophageal rather than transthoracic echocardiography.
If atrial fibrillation, develops this is a medical emergency as very rapid ventricular rates can develop Rate control with drugs or AV node ablation Ablation for Cardiac Arrhythmia The need for treatment of arrhythmias depends on the symptoms and the seriousness of the arrhythmia. Treatment is directed at causes. If necessary, direct antiarrhythmic therapy, including antiarrhythmic Sometimes rhythm control with synchronized cardioversion Rhythm control Atrial fibrillation is a rapid, irregularly irregular atrial rhythm.
If a significant underlying disorder is suspected, patients with new-onset atrial fibrillation may benefit from hospitalization, but those with recurrent episodes do not require hospitalization unless other symptoms suggest the need for it. Once causes have been managed, treatment of atrial fibrillation focuses on ventricular rate control, rhythm control, and prevention of thromboembolism. Beta-blockers eg, metoprolol , esmolol are preferred if excess catecholamines are suspected eg, in thyroid disorders, exercise-triggered cases.
Nondihydropyridine calcium channel blockers eg, verapamil , diltiazem are also effective. Digoxin is the least effective but may be preferred if heart failure Heart Failure HF Heart failure HF is a syndrome of ventricular dysfunction. These drugs may be used orally for long-term rate control.
When beta-blockers, nondihydropyridine calcium channel blockers, and digoxin —separately or in combination—are ineffective, amiodarone may be required. Patients have sudden episodes of palpitations that begin and In patients with heart failure or other hemodynamic compromise directly attributable to new-onset atrial fibrillation, restoration of normal sinus rhythm is indicated to improve cardiac output.
In other cases, conversion of atrial fibrillation to normal sinus rhythm is optimal, but the antiarrhythmic drugs Drugs for Arrhythmias The need for treatment of arrhythmias depends on the symptoms and the seriousness of the arrhythmia.
Conversion to sinus rhythm does not eliminate the need for chronic anticoagulation. For acute conversion, synchronized cardioversion Cardiac Resynchronization Therapy CRT The need for treatment of arrhythmias depends on the symptoms and the seriousness of the arrhythmia. Anticoagulation should be continued for at least 4 weeks after cardioversion. Many patients need chronic anticoagulation see Long-term measures to prevent thromboembolism Long-term prevention of thromboembolism Atrial fibrillation is a rapid, irregularly irregular atrial rhythm.
When possible, give anticoagulation before attempting to convert atrial fibrillation to sinus rhythm. However, even after strict blood pressure control, this heart rhythm abnormality can be deadly.
Vibhu Parcha, M. Atrial fibrillation is the most common heart rhythm abnormality frequently seen in patients with high blood pressure and can lead to stroke, heart failure and even death. Researchers found that adults can reduce their risk of developing atrial fibrillation by 22 percent through rigorous regulation of their systolic blood pressure to less than mmHg. They also noted that, if one does develop atrial fibrillation, tighter control may not further reduce their risk for possibly serious cardiovascular disease events.
Atrial fibrillation is also known as AF or AFib. If you have AFib, the two upper chambers of your heart, known as your atria, beat out of rhythm with the lower chambers.
AFib is a serious diagnosis. Two of the most common complications of AFib are stroke and heart failure, both of which can be fatal if not managed quickly and effectively. A stroke occurs when a blood vessel that carries blood to your brain becomes blocked.
This prevents oxygen-rich blood from reaching your brain. When your brain is deprived of oxygen, it can be permanently damaged. This can result in lasting disability or even death. According to the American Heart Association , people with AFib are about five times more likely to experience a stroke than the average person. These clots can travel to your brain, become lodged in narrow blood vessels, and cause a stroke.
If you think you may be having a stroke, call or other emergency number. Or find someone who can get emergency medical help for you. Getting immediate medical attention is essential. These classifications are relevant clinically with respect to outcomes and prognosis with rhythm-controlling treatment strategies. Atrial fibrillation is commonly associated with other supraventricular arrhythmias, namely atrial flutter and focal atrial tachycardia.
Atrial fibrillation is the most common sustained cardiac tachyarrhythmia encountered by clinicians worldwide. An estimated 2. Atrial fibrillation may be acutely associated with physiologic stressors such as surgical procedures, pulmonary embolism, chronic lung diseases, hyperthyroidism, and alcohol ingestion.
Disease states commonly associated with AF include hypertension, valvular heart disease, CHF, coronary artery disease, Wolff-Parkinson-White syndrome, pericarditis, obstructive sleep apnea, and cardiomyopathy. Considerable research has been devoted to the mechanisms and pathogenesis of AF. Genetic studies have identified specific associations, particularly in the cases of familial AF 4 Achieving a complete understanding of AF is limited by the complexity of this disorder and the heterogeneous patient population it affects.
The pathogenesis of AF can be broadly divided into the categories of triggers, substrate, and sustaining mechanisms. Since the late s, it has been recognized that the initiation of AF can occur because of premature atrial contractions triggered by beats that arise from the pulmonary veins PVs , usually from muscular tissue sleeves near the junction with the left atrium.
Focal triggers outside the PV including posterior left atrial, ligament of Marshall, coronary sinus, venae cavae, septum, and left atrial appendage contribute to the disease process.
Focal triggers, especially the PVs, are felt to be very important early in the disease process and, in particular, among patients with paroxysmal AF. Over time, myocardial fibrosis develops within the atrial tissue in association with AF to support its maintenance by shortening affected tissue refractory periods. Myocardial fibrosis of the atrium seems to be the common feature of the progression of AF disease state.
This has led to the adage that AF begets AF. Once AF is initiated by focal triggers, several theories have been postulated to explain the maintenance of AF. They include the multiple wavelet model, AF rotors and the role of the autonomic nervous system.
The multiple wavelet model has suggested that AF is sustained by multiple simultaneous wavelets meandering throughout the atria. Atrial tissue with abnormal electrical propagation recorded by mapping catheters has been referred to as complex fractionated electrograms.
Expression of specific connecting protein channels at the cellular level are also felt to be important contributors to the disease substrate and sustaining mechanisms. Contemporary understanding of the AF substrate and sustaining mechanisms now also includes the role of the autonomic nervous system and, more recently, the discovery and evaluation of the concept of AF rotors.
Cardiac ganglionic plexuses clustered posteriorly and superiorly to the left atrium are known to play an important role in the initiation and maintenance of AF. Both parasympathetic and sympathetic limbs can provoke atrial arrhythmias. Evidence supportive of this concept includes therapeutic benefit derived from destruction of cardiac ganglionic plexuses and also noncardiac plexuses including the stellate ganglion and perinephric ganglia associated with the renal arteries.
Atrial fibrillation rotors represent an emerging concept as a sustaining mechanism for AF involving spiral waves detected by spectral analysis of dominant frequencies recorded by intracardiac mapping catheters. Such spiral waves can be conceptualized as wavelets of consistent electrical activation around a central localized source that could be either structural ie, scar-related or purely functional ie, conduction heterogeneity involving certain cellular sodium and potassium channels.
The focal impulse and rotor modulation computational mapping system is used to identify AF rotors. Atrial fibrillation may have hemodynamic consequences. It can decrease cardiac output due to ineffectual atrial systole and increase pulmonary venous pressure resulting in heart failure.
Deleterious hemodynamic effects also include nonphysiologic tachycardia, increased valvular regurgitation, and irregularity in ventricular systole.
AF is associated with morbidity and even mortality. AF can produce bothersome symptoms that affect quality of life, but patients with AF also have a substantial risk of thromboembolic stroke, AF is associated with a fivefold increased risk of stroke, threefold risk of heart failure.
The clinical manifestations of AF are variable, although fatigue is the most common symptom. Often, the symptoms are attributable to the rapid ventricular response. However, even when the ventricular response is controlled, symptoms can occur from loss of AV synchrony or atrial systole This is particularly important for patients with left ventricular dysfunction CHF and impaired diastolic filling mitral stenosis , hypertrophic and restrictive cardiomyopathy. That said, some patients with AF are genuinely asymptomatic, even at rapid heart rates for unclear reasons.
More often, however, patients report nonspecific symptoms such as fatigue, dyspnea, dizziness, and diaphoresis. Palpitations are a common feature.
Occasionally, patients present with extreme manifestations of hemodynamic compromise, such as chest pain, pulmonary edema, or syncope. The clinician must realize that an irregular pulse detected by physical examination or an irregular ventricular rhythm seen on the electrocardiogram ECG is not always AF.
It is necessary to consider and exclude other types of irregular rhythm disturbances, including atrial or ventricular ectopy, atrial tachycardia, or atrial flutter Figure 1 with variable AV conduction, multifocal atrial tachycardia Figure 2 , and wandering atrial pacemaker. Conversely, a regular pulse or rhythm does not exclude AF.
For example, AF can manifest with a regular ventricular response in the presence of AV block or with a ventricular paced rhythm. Electrocardiographic findings in AF include the absence of P waves and the presence of low-amplitude, high-frequency atrial fibrillary waves F waves. The atrial rate varies in the range of to beats per minute. In the absence of drug therapy, a patient with normal AV conduction has an irregularly irregular ventricular rhythm and often has a ventricular rate in the range of to beats per minute.
This activity may resemble atrial flutter, but it is not as uniform wave to wave as atrial flutter. Most patients presenting with AF are not critically ill. However, in some cases, the presence of AF may cause life-threatening hemodynamic compromise. It should be emphasized that for any unstable patient presenting with AF—for example, a patient with chest pain, pulmonary edema, or hypotension—the recommended therapy is rapid electrical cardioversion, according to the Advance Cardiovascular Life Support guidelines.
Atrial fibrillation has particular importance in the setting of the Wolff-Parkinson-White syndrome. Patients with Wolff-Parkinson-White syndrome may be vulnerable to ventricular fibrillation and sudden death because of the development of AF, which can result in extremely rapid conduction over the accessory pathway Figure 4. Prompt electrical cardioversion is of utmost importance for these patients.
Treatment with AV node-blocking medications such as verapamil or digoxin can facilitate rapid conduction over the accessory pathway and result in ventricular fibrillation. When intravenous pharmacologic therapy is required, the drug of choice is procainamide or amiodarone. There are 3 goals in the management of AF: control of the ventricular rate, minimization of thromboembolism risk particularly stroke , and restoration and maintenance of sinus rhythm.
The first 2 goals are essential for most patients, but the third goal may not be necessary in all patients. Rate control in patients with AF is essential to reduce symptoms and improve quality of life. The optimal heart rate goal has not been fully defined and may be patient specific. In the RACE II clinical trial, patients were randomly assigned to strict less than 80 bpm vs lenient less than bpm rate control strategies. Based on this study, the European Society of Cardiology guidelines incorporated the lenient rate control strategy as the first-line approach to asymptomatic patients with preserved cardiac function.
Guideline statements only address goals in patients with preserved cardiac function. The optimal rate in patients with heart failure has not been fully defined.
For example, some studies show that in patients with heart failure, slow ventricular rates are associated with higher mortality and higher ventricular rates may be needed to improve exercise tolerance. Hence, most clinicians use a patient-specific window of optimal rate control that avoids the consequences of both extreme bradycardia and tachycardia. The most commonly used drug classes are beta blockers and calcium channel blockers.
Most patients with persistent atrial fibrillation receive daily suppressive therapy. However, a pill-in-the-pocket, rate-control strategy has been proposed in patients with a low burden of self-terminating AF, though no studies have investigated this strategy. If these medications are ineffective or if excessive bradycardia occurs, other measures may need to be considered.
One option suitable for some patients is catheter ablation of the AV node and pacemaker implantation ablate and pace. Meta-analysis of the ablate-and-pace approach has demonstrated improvements in a number of clinical parameters, including symptoms, quality of life, exercise function, cardiac performance, and longevity in patients with CHF receiving a biventricular pacemaker.
However, this approach usually results in pacemaker dependence and carries the associated risks and complications of indwelling pacemaker leads. Pacemaker implantation without AV nodal ablation should be considered if the problem is simply excessive bradycardia that prohibits the effectiveness of rate-controlling medication, and the rapid ventricular rates are well controlled by medication. For patients with abnormal LV systolic function, a biventricular pacemaker ie, cardiac resynchronization therapy should be considered in conjunction with AV nodal ablation based on the results of the BLOCK HF trial.
Includes data from January et al 1 and Van Gelder et al. In patients with an implantable cardioverter defibrillator, great care is needed in both the device programming and pharmacologic rate control in order to avoid the risk of inappropriate shocks associated with rapid ventricular rates. Atrial fibrillation carries a considerable risk for thromboembolism and stroke.
The Framingham study has shown that during a follow up period of 30 years, patients with nonvalvular AF had a more than fivefold risk of stroke and the risk of stroke attributed to stroke increased with age. Ischemic strokes related to AF tend to be associated with greater morbidity and mortality than from other causes of stroke.
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