Atrial fibrillation is a fibrillation of the atria, atrial fibrillation accounts for about 4% of the adult population, such a high incidence is a bit scary, in the end atrial fibrillation is what is going on?
I. What is atrial fibrillation?
Atrial fibrillation is defined as disorderly, asynchronous electrical activity occurring in the atrial tissue, it is the most common arrhythmia, according to statistics, atrial fibrillation accounts for about 4% of the adult population, atrial fibrillation is a typical disease of the elderly, the older the age, the higher the chance of disease, people over 80 years old can reach 30%. Atrial fibrillation comes from a large amount of folded excitation, resulting in extreme excitation of the atria, with abnormal beats emitted at 400 to 600 beats/min, leading to atrial fibrillation rather than contraction.
The ventricles respond only to those impulses that pass through the AV node, and on the ECG, atrial activity is no longer represented by P waves, but is replaced by a baseline wave called an f wave. This rhythm can be paroxysmal or sustained, and can be caused by or be the result of atrial prematureness.
Second, how does atrial fibrillation occur?
1, Atrial fibrillation can occur in: heart surgery, chronic hypotension, pulmonary embolism, COPD, electrolyte disturbances, mitral stenosis or insufficiency, hyperthyroidism, infection, coronary artery disease, acute myocardial infarction, pericarditis, hypoxia or atrial septal defect.
2. It can occur in healthy individuals under the following conditions.
Excessive use of caffeine, alcohol, nicotine, etc.
Use of certain drugs such as, aminophylline, digoxin, etc.
Catecholamines released during exercise can also stimulate arrhythmias.
3. Where did the atrial rhythm go?
Loss of atrial rhythm, accelerated ventricular rate, and shortened ventricular filling time can lead to significant clinical conditions. If the ventricular rate is >100 beats/min, called uncontrolled atrial fibrillation, patients can experience heart failure, angina, or syncope; patients with known heart disease, such as hypertrophic cardiomyopathy, mitral stenosis, rheumatic valve disease, and mitral valve replacement, tend to respond worse to atrial fibrillation and can go into shock or severe heart failure.
If left untreated, atrial fibrillation can lead to cardiovascular collapse, thrombosis, and systemic arterial or pulmonary embolism.
4. Is there a risk when atrial fibrillation turns into sinus rhythm?
Patients with atrial fibrillation are at increased risk of atrial thrombosis and systemic arterial embolism because the atria do not contract and blood pressure pools in the atrial wall, where clots can form. If sinus rhythm is restored and the atria begin to contract, the clot can dislodge from the atrial wall and travel through the pulmonary or body circulation, leading to catastrophic consequences. Embolism to the brain causes stroke.
Third, how to monitor atrial fibrillation?
1. The wonderful “filtering” effect of the atrioventricular junction.
At an atrial rate of 400-600, the atrioventricular node protects the ventricles from the effects of rapid atrial rhythm, in a way that “filters” and blocks some of the atrial excitation. The atrioventricular node itself does not receive all excitation, and if the tissue surrounding the atrioventricular node is in a state of inactivity, impulses from other parts of the atrium cannot reach the atrioventricular node, a mechanism that reduces impulse conduction through the atrioventricular node to the ventricles.
Atrial fibrillation is considered to be controlled when the ventricular rate is <100 beats/minute and uncontrolled when the ventricular rate is >100 beats/minute.
2. Pulse differences.
When examining an AF or, you can find that the radial artery pulses are slower than the atrial pulses because the weaker heart contractions are not sufficient to produce palpable peripheral arterial pulses. The pulse rhythm is irregular, and if the ventricular rate is fast, the patient may show signs and symptoms of decreased cardiac output, such as low blood pressure, or dizziness. If atrial fibrillation persists and becomes chronic, the heart may compensate for this decrease in cardiac output, but there is an increased risk of embolism in other areas such as the lungs, brain, and
IV. How to manage atrial fibrillation.
1. Primary treatment goals.
Reduce the ventricular response and control the ventricular rate to less than 100 beats/min. Medication or electrical cardioversion, drugs plus electrical cardioversion can be used to convert atrial fibrillation to sinus rhythm.
2. Timing is everything.
The use of electrical resuscitation within 48 hours of atrial fibrillation is successful in most cases, while the success rate decreases beyond 48 hours, and patients should be treated urgently if they have angina pectoris or manifestations of decreased cardiac output. When atrial fibrillation is acute, the vagus nerve manipulation method or carotid sinus massage is used to slow down the ventricular rate, but not to transcend the rhythm.
3. Transthoracic rhythm.
Symptomatic patients require immediate synchronized electrical cardioversion. Patients must first receive appropriate anticoagulation because conversion to sinus rhythm can cause thromboembolism, especially in patients with chronic or paroxysmal atrial fibrillation.
Conversion to sinus rhythm can cause a sudden return of vigorous contraction of the atria, and if a thrombus has formed in the atria, the return of contraction can lead to embolization of the arterial system. Embolism to the brain causes stroke.
4. Restoration of the sinus node.
Drugs can be used to maintain sinus rhythm after cardioversion and to control ventricular rate in chronic atrial fibrillation. Digoxin, procainamide, tretinoin, etanercept, isobodine, etc. Some of these drugs prolong the atrial inactivity period so as to give the sinus node a moment to re-establish its role as a pacemaker, while other drugs that slow down atrioventricular node conduction can control ventricular rate.
Radiofrequency ablation may be considered in symptomatic atrial fibrillation that does not respond to conventional therapy. To evaluate a patient with atrial fibrillation, look for peripheral pulses and apical beats, and if unmonitored, note the difference between irregular pulses and apical beats. Evaluate patients with symptoms with reduced cardiac output and heart failure. Patients are recorded to report changes in heart rate, syncope or head fascination, chest pain, and signs of heart failure such as dyspnea and peripheral edema.