Atrial fibrillation

Introduction to atrial fibrillation Atrial fibrillation (Af), abbreviated as atrial fibrillation, is one of the most common arrhythmias, and is caused by a number of small reentry rings caused by atrial-dominant reentry rings. The overall incidence of atrial fibrillation is 0.4%, and the incidence of atrial fibrillation increases with age, reaching 10% in people over 75 years of age. The frequency of atrial excitement in atrial fibrillation is 300~600 beats/min. The heartbeat frequency is often fast and irregular. Sometimes it can reach 100~160 beats/min. It is not only much faster than normal people's heartbeat, but also absolutely not neat, the atrium is lost. Effective shrinkage function. Large-scale investigations in China have shown that the prevalence of atrial fibrillation is 0.77%, the prevalence of atrial fibrillation in men (0.9%) is higher than that in women (0.7%), and the prevalence of atrial fibrillation above age 80 is 7.5%. In addition, the increase in the prevalence of atrial fibrillation is also closely related to the growth of coronary heart disease, hypertension and heart failure. Atrial fibrillation will become one of the most prevalent cardiovascular diseases in the next 50 years. basic knowledge The proportion of illness: 20% (20% of heart patients) Susceptible people: no special people Mode of infection: non-infectious Complications: peripheral arterial embolism, sudden death, arrhythmia

Cause of atrial fibrillation

Organic heart disease (35%):

Such as pulmonary heart disease (incidence rate of 4% to 5%, mostly paroxysmal, decreased respiratory function after the improvement), chronic constrictive pericarditis; congenital heart disease, etc., atrial fibrillation is self-discipline Increased focal origin of atrial fibrillation, and part of paroxysmal and partial persistent and chronic atrial fibrillation caused by local micro-reentry mechanism in the atrium, pulmonary veins, and vena cava.

Pre-excitation syndrome (20%):

It may be due to the short-term refractory period of patients with pre-excitation syndrome. Once the reentry conditions are established, the impulses through the bypass increase, and this impulse can be induced to atrial fibrillation after re-entry into the left atrial stress period. The incidence of atrial fibrillation is 11.5% to 39%. Pre-excitation syndrome complicated with atrial fibrillation is considered to be serious because the bypass does not have the protective effect of physiological conduction delay like the atrioventricular node, so the ventricular rate is transmitted by the bypass. More than 180 beats / min, seriously affecting the blood output of the heart.

Other diseases (15%):

Alcoholism and smoking, emotional excitement, excessive smoking, urination, etc. can occur directly or induce atrial fibrillation based on the original heart disease.

Familial atrial fibrillation (10%):

Due to gene mutation, the genetic pattern belongs to AD inheritance, which occurs mostly after adulthood, and is paroxysmal. Atrial fibrillation occurs and terminates unconsciously. The symptoms of atrial fibrillation are mild, mostly caused by fatigue, mental stress, infection, Pain, drinking, smoking, etc., the heart function remains normal, and the general prognosis is good.

The reason is unknown (5%):

Idiopathic atrial fibrillation in healthy people often has no basis for organic heart disease.

Cause:

(1) Rheumatic heart disease: about 33.7% of the cause of atrial fibrillation, more common with mitral stenosis and insufficiency.

(2) Coronary heart disease: Coronary angiography confirmed coronary heart disease with angina pectoris, the incidence of atrial fibrillation was 1.5%, the incidence of atrial fibrillation in old myocardial infarction was 3.8%; the incidence of acute myocardial infarction was 8.2%, and The incidence of atrial fibrillation was 11% in patients with normal coronary arteries confirmed by coronary angiography due to chest pain. In general, the incidence of coronary heart disease was lower.

(3) Hypertensive heart disease: Many small arterial lumens of the atrial muscle may be narrowed or completely occluded due to thickening of the intima, causing ischemic changes and fibrosis of the local myocardium.

(4) Hyperthyroidism: focal myocardial necrosis and lymphocytic infiltration in early myocardium, myocardial often with small localized fibrosis, the incidence rate is 5%, more common in patients aged 40 to 45 years, young patients are less common Even if it happens, it is mostly paroxysmal.

(5) Sick sinus syndrome: When the sinus node arteries have focal dysplasia of the muscle fibers, abnormal collagen structure and degeneration around the sinus node, especially the sinus node degeneration and sinus impulse abnormalities, can promote The occurrence of atrial fibrillation.

(6) Cardiomyopathy: all types of cardiomyopathy, often accompanied by focal atrial muscle inflammation, degeneration or fibrosis, atrial enlargement easily lead to atrial fibrillation, in patients with alcoholic cardiomyopathy, atrial fibrillation is often the disease The initial performance, the incidence is high.

(7) Systemic invasive diseases: systemic lupus erythematosus, scleroderma, leukemia, amyloidosis, etc.

(8) Lung and systemic infections as well as chronic pulmonary insufficiency.

(9) Heart surgery and trauma.

(10) Digitalis poisoning, aconitine, nicotine and other poisoning can induce atrial fibrillation.

(11) Various cardiac catheterization and transesophageal electrical stimulation, and cardioversion can directly induce atrial fibrillation.

Pathogenesis

It is currently believed that most paroxysmal atrial fibrillation and some persistent or chronic (permanent) atrial fibrillation are autologously elevated focal atrial fibrillation; some paroxysmal and partially persistent and chronic atrial fibrillation are In the atrium, pulmonary veins, vena cava local micro-reentry mechanism.

1. Localized atrial fibrillation with increased autonomy

Most scholars believe that the focal electrical activity that can trigger atrial fibrillation may be abnormal autonomic increase or trigger activity. The focal has significant anatomical features. Most of the focal points are located in the pulmonary veins, and a few are located outside the pulmonary veins. Pacemaker cells, T, P cells and Purkinje cells.

(1) Pulmonary vein: About 95% of the foci of atrial fibrillation triggered by focal origin atrial fibrillation are located in the bilateral superior pulmonary veins, 48% to 51% of the left superior pulmonary veins, and 26% to 44% of the right superior pulmonary veins. Bilateral lower pulmonary veins accounted for 28%, and in most patients with focal atrial fibrillation, 68% had two or more pulmonary veins with a triggering focal point; or two focal sites were located in the same pulmonary vein. Only 32% are located in a single pulmonary vein, a feature that increases the difficulty of successful ablation.

(2) superior vena cava: About 6% of patients trigger atrial fibrillation in the superior vena cava, and the focal point is located at the junction of the right atrium and superior vena cava (19 ± 7) mm.

(3) right atrium: located in the right atrium accounted for 3% to 4.7%, can be located in the right atrial side wall, at the interatrial septum.

2. Foldback mechanism

The atrial muscle sleeve of the pulmonary vein is present in the autopsy of patients with and without paroxysmal atrial fibrillation. The distal fibrosis of the muscle sleeve is increased, and finally the atrophic muscle cells disappear in the fibrous tissue, which constitutes the basis of micro-reentry. In addition, it is also found that the focal electrical impulse (from the pulmonary vein or vena cava) is slowly transmitted to the left atrium or right atrium (up to 160ms), and there is significant diminished conduction, irregular micro-reentry in the atria, the reentry loop cannot Make sure that atrial overspeed pacing cannot be terminated.

3. Two modes of triggering and driving atrial fibrillation

1 The electrical activity released by the focal area triggered atrial fibrillation, and the subsequent atrial fibrillation was not related to the focal electrical activity. This mode accounted for the majority, called the focal trigger mode; 2 the focal presence of a long, continuous discharge caused Atrial fibrillation, called focal drive mode, is rare, the relationship between the two modes, the difference in the mechanism of occurrence is unclear, such as the persistence of atrial fibrillation, there are multiple driving and triggering mechanisms coexisting or alternating, muscle sleeve tissue The electrical activation can be fast or orderly or fast.

4. The role of pulmonary vein dilatation

The atrial fibrillation group was found to contain focal pulmonary veins larger than other pulmonary veins, approximately 1.64 cm: 1.07 cm.

The matrix of atrial fibrillation refers to the underlying causes of its occurrence, including three aspects: 1 anatomical matrix: including fibrosis of atrial muscle, atrial dilatation, atrial infarction, atrial surgery, etc., the formation of anatomical matrix needs to be longer Time, some may take several years, 2 functional matrix: including atrial stretch and ischemia, autonomic nerve and drug effects, bradycardia or excessive speed, the formation of functional matrix takes a relatively short time, Formed in days or months, 3 start factors: including cardiac arrest, long and short period phenomenon, short and long period phenomenon, etc., starting factors may be formed in seconds to minutes.

In addition to the presence of the matrix, atrial premature contraction is required as a trigger to cause atrial fibrillation. The single atrial premature contraction triggers about 45%, and the multiple atrial premature contraction triggers about 19%. Short-term atrial tachycardia triggered atrial fibrillation, accounting for about 24%.

Atrial fibrillation induced by one or more relatively limited and fixed focal recurrent episodes of pre-atrial contraction or atrial tachycardia is called focal originated atrial fibrillation.

Atrial fibrillation can be converted from paroxysmal to persistent, in addition to aggravation of the disease, but also related to the electrical remodeling of the atrial myocytes themselves, ie the electrical remodeling of the atrial muscle.

Atrial fibrillation prevention

1. Prevention of atrial fibrillation should begin to treat primary heart disease from the prevention and treatment of causes and causes, and control the factors that induce atrial fibrillation.

2. After atrial fibrillation is converted, antiarrhythmic drugs are usually needed to maintain sinus rhythm to prevent recurrence of atrial fibrillation. In recent years, special procedures embedded in pacemakers have been used to control and prevent atrial fibrillation, which is already in cardiovascular disease. Significant curative effects have been achieved in the field of prevention and treatment, making some of the original drugs refractory and recurrent episodes of atrial fibrillation to be satisfactorily controlled.

3. The current discovery of human atrial fibrillation genes will also open up new ways to prevent atrial fibrillation in the future.

Atrial fibrillation complications Complications, peripheral arterial embolism, sudden cardiac arrhythmia

There may be complications such as cerebral artery embolism, peripheral arterial embolism, pulmonary embolism, cardiac insufficiency, and sudden cardiac death.

1. Cerebral artery embolization: one of the most common complications of atrial fibrillation, epidemiological statistics, the incidence of stroke in patients with atrial fibrillation is 2% to 6%, and 75% of patients with atrial fibrillation complicated with systemic embolism are cerebral arteries. Embolism, embolus of cerebral embolism mainly comes from the left atrium and the auricle, 75% of the embolus comes from the left atrial wall thrombus, and 25% from the atherosclerotic plaque.

2. Peripheral arterial embolization: 80% of patients with peripheral arterial embolism have atrial fibrillation. After atrial fibrillation with atrial fibrillation, the arterial blood flow to the distal end of the systemic circulation causes acute arterial embolism.

3. Pulmonary embolism: The thrombus of the right heart in patients with atrial fibrillation causes pulmonary embolism in the embolism of the pulmonary artery and its branches. The mortality rate of pulmonary embolism is as high as 20% to 40%. In the United States, there are 50,000 to 100,000 patients with pulmonary embolism every year. Ranked third in the cause of death in the United States.

4. Cardiac insufficiency: The ventricular rate of atrial fibrillation is closely related to the state of cardiac function. When atrial fibrillation and rapid ventricular rate, especially when the cardiac function is poor, the cardiac output is significantly reduced, leading to tissue and organs. Insufficient perfusion and acute congestion syndrome can be complicated by acute heart failure, and clinically, acute left heart failure is more common.

5. Sudden cardiac death: rapid atrial fibrillation, increased ventricular rate, reduced effective cardiac output, decreased coronary perfusion, can lead to cardiac arrest, the main causes of sudden cardiac death caused by atrial fibrillation: atrial fibrillation with pre-excitation Signs; pulmonary embolism; acute cardiac insufficiency; nerves, mental factors, etc.

Symptoms of atrial fibrillation Common symptoms Angina pectoris Chest boring cerebral hypoxia, weak heartbeat, palpitations, palpitation, myocardial infarction, tachycardia, arrhythmia

First, clinical manifestations

1. Clinical manifestations of patients with paroxysmal atrial fibrillation

(1) Male patients are more common: there is often no organic heart disease.

(2) Paroxysmal atrial fibrillation can occur frequently, and the dynamic electrocardiogram shows that the episode lasts from several seconds to several hours.

(3) often accompanied by frequent atrial premature contraction, atrial premature contraction can induce atrial fibrillation.

(4) Most of the inter-term atrial contraction of the atrial premature contraction <500ms, often P-on-T phenomenon, and induced short-term atrial fibrillation.

(5) Asymmetry, exercise and other sympathetic nerves can induce episodes of atrial fibrillation.

(6) The incidence of atrial fibrillation in patients with focal atrial fibrillation with relatively low age is relatively small, and the atrium is often not large, most of which is a pulmonary vein involvement.

(7) When paroxysmal atrial fibrillation occurs, if the frequency is not fast, there may be no obvious symptoms, such as rapid heart rate, patients complaining of heart palpitations, palpitation, chest tightness, shortness of breath, heart jumping, irritability, fatigue, etc., auscultation of arrhythmia, heart sounds Weaknesses, slowness and shortness of veins, polyuria, etc., such as too fast ventricular rate can cause blood pressure to drop or even syncope.

2. Clinical manifestations of patients with persistent and chronic atrial fibrillation

(1) The symptoms of persistent (or chronic) atrial fibrillation are related to basic heart disease, and also related to the rate of ventricular rate. There may be palpitations, shortness of breath, chest tightness, fatigue, especially after physical activity, ventricular rate increases significantly, and syncope may occur. Especially in elderly patients, due to cerebral hypoxia and vagus nerve hyperactivity.

(2) irregular heart rhythm: the first heart sound is uneven, the interval is different, the untreated atrial fibrillation ventricular rate is generally 80 ~ 150 times / min, rarely more than 170 times / min, heart rate > 100 times / min , said rapid atrial fibrillation; >180 times / min called extreme atrial fibrillation, with short pulse.

(3) can induce heart failure or increase the original heart failure or basic heart disease, especially when the ventricular rate exceeds 150 times / min, can aggravate myocardial ischemia symptoms or induce angina.

(4) Increased susceptibility to thrombosis, which is prone to embolic complications. Atrial fibrillation lasts for more than 3 days. There may be thrombosis in the atria, age, organic heart disease, enlarged left atrial diameter, and plasma fibers. Increased protein is a risk factor for thromboembolic complications.

Second, the special type of atrial fibrillation:

1. Vagus-mediated atrial fibrillation (referred to as vagus atrial fibrillation)

Various arrhythmias are affected by the autonomic nervous system, but the degree is different. Animal experiments confirm that stimulation of the vagus nerve can induce atrial fibrillation. In 1978, Coumel proposed vagus-mediated atrial fibrillation, which has been confirmed to be not uncommon. Its characteristics are as follows:

(1) Clinical features:

1 The first author is 30 to 50 years old, with an age range of 25 to 65 years old and a male to female ratio of 4:1.

2 almost exclusively occurs in patients without structural heart disease.

3 Most patients often take several years of drug treatment, but the curative effect is poor, and the condition is aggravated before the diagnosis. The clinical history is often 2 to 15 years.

(2) Characteristics of the attack mode:

1 The episode is mostly at night, when resting, rarely or never occurs during physical activity or emotional excitement.

2 seizures are often associated with eating, especially after dinner, because of breakfast, lunch, sympathetic activity is strong, drinking is a triggering factor, paroxysmal atrial fibrillation mainly occurs at night, often in the morning to restore sinus rhythm.

3 mechanical or drug stimulation excitement vaginalism can often induce atrial fibrillation.

4 Almost all patients tend to have frequent episodes with the progress of the disease: usually from the annual attack several times to the monthly, weekly, or even several times a day, the duration of the attack gradually extends from a few minutes to several hours, all of which are paroxysmal atrium. There is no or little change into persistent atrial fibrillation.

(3) ECG features:

1 The sinus rhythm can be slowed down before the onset, showing sinus bradycardia (indicating increased vagal activity), which lasts for several hours or several cardiac cycles, and only occurs when a certain critical degree is reached. The critical heart rate of most cases is 60. Less than / min.

2 In addition to the slowing of the heart rate, a few minutes or tens of minutes before the onset, often atrial premature contraction or atrial premature contraction.

3 During the attack, atrial fibrillation and type I are often seen, and atrial flutter alternates, or mixed.

4 years of follow-up did not develop into sick sinus syndrome.

5 vagus nerve can shorten the action potential and refractory period of atrial myocytes, and with the attenuation of excitatory conduction in the room, so atrial fibrillation can also be induced by pre-atrial contraction that is not very advanced.

(4) Treatment:

1 drug treatment: most anti-arrhythmia drug treatment is a feature of vagal atrial fibrillation, digitalis can not prevent atrial fibrillation, but promote its occurrence, verapamil or beta-blockers can make its attacks more frequent Therefore, they are all banned. The IA drugs are effective at first. When the treatment time is long, the treatment is ineffective due to drug resistance. The effective rate of pirimidin and quinidine is more than 20%. The former has a more obvious effect, and the effective rate of amiodarone is up to 40% to 50%, it is currently considered that the combination of flecainide and amiodarone is effective, but there are still a considerable number of cases that are ineffective, frequent attacks, and obvious symptoms.

2 atrial pacing therapy: In recent years, it has advocated the placement of artificial cardiac pacemakers (permanent). In addition to obvious hemodynamic benefits, pacing therapy also has obvious antiarrhythmic effects. AAI pacemakers are often used. DDD pacemakers are used when there is atrioventricular node dysfunction or bundle branch block.

2. Sympathetic-mediated paroxysmal atrial fibrillation

Has the following characteristics:

(1) In patients without structural heart disease, the incidence of atrial fibrillation is significantly lower than that of vagus nerve-mediated paroxysmal atrial fibrillation, rarely seen in hyperthyroidism, pheochromocytoma Such patients, some scholars believe that paroxysmal atrial fibrillation in organic heart disease is mostly sympathetically mediated.

(2) No age, gender difference.

(3) Daytime hair as a main feature, especially in the morning, often in mood swings or exercise.

(4) often accompanied by polyuria, frequent urination symptoms.

(5) History or dynamic electrocardiogram records show that sinus beats accelerate before the onset of atrial fibrillation, up to 90 beats/min.

(6) There is a mixture of atrial fibrillation and atrial tachycardia in the episode, and there is rarely a typical atrial flutter.

(7) Sympathetic stimulants (such as isoproterenol, etc.) can induce their onset.

(8) Optional beta blockers, digoxin, IA or IC antiarrhythmic drugs and amiodarone treatment.

(9) Atrial pacing therapy is ineffective.

3. Atrial fibrillation with differential conduction in the room

At the time of atrial fibrillation, the QRS wave pattern can be normal or abnormal. The abnormal QRS wave can be caused by simultaneous bundle branch block, pre-excitation syndrome or indoor differential conduction. The rate of atrial fibrillation is fast due to ventricular rate. Irregular, often: 1 Ashman phenomenon, that is, a short interval of QRS waves after a long RR interval has a single differential conduction; 2 atrial fibrillation with a differential conduction of the phenomenon of atrial fibrillation than atrial flutter and atrial tachycardia Overspeed is more likely to produce indoor differential conduction.

ECG characteristics of atrial fibrillation with differential conduction in the room:

(1) The shorter the interval between the QRS wave and the previous QRS wave between the atrial fibrillation and the indoor differential conduction, the wider the deformity, and the interval between the joints is not fixed, and the RR interval in front of the differentially transmitted QRS wave The longer it is, the more likely it is to be deformed, that is, the deformed QRS complex has a long interval and a short-term interval.

(2) The QRS wave of the indoor differential conduction is mostly the right bundle branch block type, and the V1 lead is mostly the three-phase QRS wave group. The QRS wave has the same starting vector as the normal descendant, and the indoor differential conduction Sometimes it can also be a left bundle branch block type, in which the r wave of the V1 lead is smaller than the r wave without differential conduction.

(3) In the case of indoor differential conduction, the malformed QRS wave has no fixed interval (matching interval), and there is no compensatory interval thereafter.

(4) QRS wave malformation during indoor differential conduction occurs more frequently in the case of ventricular rate, and disappears after the ventricular rate is slowed down.

(5) Different degrees of QRS wave broadening and deformation can be seen on the same lead.

(6) When atrial fibrillation is accompanied by differential conduction cascading, the QRS wave time limit is mostly 0.12~0.14s. Occasionally, atrial fibrillation is accompanied by differential conduction in the left bundle branch block pattern (more than 3 phase resistance in the left bundle branch) Delayed time), QRS time limit can be >0.14s, but <0.16s, such as >0.16s is ventricular tachycardia, atrial fibrillation with indoor differential conduction cascading phenomenon, if measures can be taken to slow the atrioventricular conduction, slow down Ventricular rate, differential conduction can be terminated.

4. Pre-excitation syndrome with atrial fibrillation

(1) The incidence rate is higher: the dominant pre-excitation syndrome has a higher incidence of atrial fibrillation than the recessive pre-excitation syndrome.

(2) Mechanism: It is not clear that there are three possibilities: 1 Atrioventricular reentry tachycardia caused by pre-excitation syndrome, due to excessive ventricular rate, can cause atrial myocardium ischemia and cardiac instability caused by atrial micro Atrial fibrillation occurred after reentry; 2 ventricular premature contraction was retrogradely transmitted to the atria by the atrioventricular bypass to atrial fibrillation; 3 anterior conduction refractory period was prone to atrial fibrillation.

(3) Clinical features:

1 ventricular rate is very fast: more rapid atrial fibrillation, ventricular rate is 160 ~ 250 times / min.

2 hemodynamics is seriously affected: patients with dizziness, syncope, shock, angina pectoris, myocardial infarction, etc., and even ventricular fibrillation, A-S syndrome.

(4) The electrocardiogram has the following performances:

1 Atrial activation through the atrioventricular node: QRS wave morphology, time limit is normal, such ECG is seen in patients with occult bypass and longer refractory period of dominant bypass.

2 Atrial agitation is mostly or completely bypassed: the QRS wave of each lead is significantly increased similar to ventricular tachycardia.

3 atrial activation through the atrioventricular node and bypass transmission variable: the same lead QRS complex width and time limit are not equal, RR interval varies.

5. Atrial fibrillation reveals a potential pre-excitation syndrome

Potential pre-excitation syndrome is a special type of intermittent pre-excitation syndrome. The bypass has a pre-transmission ability, but it does not appear in the conventional electrocardiogram. It is found that this case only occurs in atrial fibrillation, or in the application of the ocean. Rehmannia only appeared when atrial fibrillation was treated. When atrial fibrillation was corrected, the pre-excitation syndrome also disappeared.

6. Atrial fibrillation combined with atrioventricular block

(1) Atrial fibrillation combined with second-degree atrioventricular block: previous diagnostic criteria: atrial fibrillation can be diagnosed when the RR interval is 1.5s or continuous RR interval is 1.2-1.5s, but some scholars report For patients who met the above diagnostic criteria, sinus rhythm appeared after electric shock cardioversion, atrial fibrillation disappeared, except for the presence of one-time atrioventricular block, most of them did not show ECG of second degree atrioventricular block, so It is considered that the above diagnostic criteria cannot be established and should be referred to as atrial fibrillation with long interval.

It has been suggested that when the above situation is accompanied by the application of digitalis in heart failure, it is considered that if the average ventricular rate is above 60 beats/min and the RR interval is more than 1.5 s, other clinical and electrocardiographic manifestations without digitalis poisoning can be continued. Use digitalis; if the average ventricular rate is <60 beats/min, and there are more long RR intervals, even if it is not digitalis poisoning, digitalis should be used with caution (not used or disabled).

(2) atrial fibrillation combined with third degree atrioventricular block: characterized by a slow and regular ventricular rate (<60 times / min) in atrial fibrillation, ventricular rate of QRS wave system supraventricular, frequency is 40 ~ At 60 times/min, it is the atrioventricular transitional rhythm; if the QRS is wide and malformed, the time limit is 0.12s, the frequency is 25~40 times/min, and the ventricular escape rhythm is absent.

7. Isolated atrial fibrillation in atrial separation

Independent atrial fibrillation is rare. When the atrium is separated (atrial separation), there is a certain limitation of the atrial muscle that atrial fibrillation cannot be transmitted to the ventricle; other parts are still controlled by the sinus node. The ventricle was controlled by the lower ventricle, and an isolated atrial fibrillation wave was observed between the PP on the electrocardiogram, forming a sinus rhythm with isolated atrial fibrillation atrial separation.

Atrial fibrillation

Mainly rely on ECG diagnosis, ECG features are as follows:

1. Typical ECG characteristics of atrial fibrillation

(1) The sinus P wave disappears in each lead, and is replaced by atrial fibrillation waves (f waves) with different shapes and different sizes, with a frequency of 350-600 beats/min.

(2) QRS wave shape, the amplitude is basically the same as the sinus rhythm, or accompanied by indoor differential conduction, but the amplitude changes greatly and varies from each other.

(3) The RR interval is absolutely uneven.

2. Characteristics of paroxysmal atrial fibrillation

(1) Atrial fibrillation lasts for a few seconds to a few minutes and can last for several hours.

(2) Before multiple episodes of atrial fibrillation, there are often multiple or single atrial premature contractions. Sometimes there is no atrial premature contraction before the onset of atrial fibrillation. It may belong to the focal ectopic discharge. The discharge needs to be through the heart. The electrogram was confirmed.

(3) Patients may have frequent premature contractions, and the total number is often >700/24h.

(4) Atrial premature contraction induced by atrial fibrillation is often similar to that of isolated atrial premature contraction. Occasionally, isolated atrial premature contractions, which may be different from each other, may be bystanders, regardless of the induction of atrial fibrillation. .

(5) The single atrial premature contraction and the first ectopic P wave that triggers atrial fibrillation often overlap in the T wave after the previous QRS wave, forming a P-on-T phenomenon.

(6) In the surface electrocardiogram of patients with focal origin atrial fibrillation, when one or more lead P waves in the II, III, and aVF leads are negatively positive and biphasic, the focal point is located in the lower pulmonary vein.

(7) The patient's electrocardiogram may have a common form of atrial flutter. At this time, the impulse of the focal release may invade the atrial flutter, causing the atrial flutter to abruptly terminate, or the atrial flutter may evolve into atrial fibrillation.

(8) After a short burst of atrial fibrillation, atrial fibrillation can occur again after a normal sinus P wave.

(9) Only one focal electrical activity can form different types of atrial arrhythmia. Single discharge can be expressed as isolated atrial premature contraction, and slower frequency repeated discharge can be expressed as autonomous atrial. Tachycardia, rapid and continuous discharge can be expressed as primary monomorphic atrial tachycardia or focal atrial flutter. These characteristics make the same patient can change and be capricious when recording dynamic electrocardiogram. Spontaneous atrial arrhythmia.

In conclusion, the electrocardiographic features of focal origin of atrial fibrillation are characterized by multiple forms of atrial arrhythmias, including atrial premature contraction, atrial tachycardia, atrial flutter and atrial fibrillation alternating, atrial premature contraction Frequently triggering atrial fibrillation, the f-wave frequency of paroxysmal atrial fibrillation is relatively slow and regular, and needs to be differentiated from atrial tachycardia.

3. ECG typing of atrial fibrillation

(1) According to the ECG f wave thickness classification:

1 coarse wave atrial fibrillation: refers to the amplitude of f wave > 0.1mV, more common in rheumatic heart disease mitral stenosis, hyperthyroidism, atrial flutter into atrial fibrillation, this type of drug, The response to electric shock cardioversion is good, the effect is good, and the recurrence rate is low.

2 fine-wave atrial fibrillation: refers to the amplitude of f wave 0.1mV, more common in patients with long-term rheumatic heart disease, coronary heart disease and other patients, this type of drug, poor response to electric shock, poor efficacy, high recurrence rate.

3 fluttering atrial fibrillation: or impure flutter.

(2) According to the rate of ventricular rate:

1 slow rate of atrial fibrillation: ventricular rate 100 beats / min, found in: A. patients with atrial fibrillation stable, or digitalis or beta blockers for the basic control of the disease, the ventricular rate can fluctuate at 70 ~ 90 times / min; B. benign atrial fibrillation in young healthy people; C. more common in the elderly due to increased vagal tone; D. patients with advanced heart failure, although heart failure is aggravating, but the heart rate is slow; Digitalis blockage caused by digitalis poisoning or hypokalemia.

2 rapid atrial fibrillation: ventricular rate of 100 ~ 180 times / min, can produce significant hemodynamic effects, seen in a variety of causes of newly occurring atrial fibrillation, with heart failure are more common.

3-speed atrial fibrillation: ventricular rate of more than 180 beats / min, more common in: A. pre-excitation syndrome with atrial fibrillation; B. quinidine in the process of conversion of atrial fibrillation, has a serious impact on hemodynamics , easily lead to heart failure or worsening heart failure, myocardial ischemia and ventricular fibrillation.

Diagnosis of atrial fibrillation

diagnosis

According to clinical symptoms and signs, atrial fibrillation can be initially diagnosed, but electrocardiogram is needed for diagnosis. It is simple and easy to perform; but for patients with a brief episode of atrial fibrillation, it is necessary to perform dynamic electrocardiogram and other tests.

Differential diagnosis

1. Differential diagnosis of atrial fibrillation with differential conduction and ventricular premature contraction

The characteristics of ventricular premature contraction are:

The QRS wave of 1V1 lead is unidirectional or bidirectional, V6 is QS or rS type; 2 is more common with left bundle branch block; 3 has fixed joint interval, followed by complete compensatory interval; 4 deformed QRS wave The starting vector is different from the normal descendant.

2. Atrial fibrillation with differentiation of indoor differential conduction and ventricular tachycardia

Most of the former rhythms are absolutely irregular:

1 The basic rule is very fast when the heart rate is extremely fast, while the latter basic rule (the RR interval is only 0.02~0.04s) or absolute rule; 2 the former QRS time limit is 0.12~0.14s, the variability is large; and the latter QRS time limit can be greater than 0.14s, such as >0.16s is definitely ventricular tachycardia, in addition to variability is small; 3 the former has no inter-trial interval and no compensatory interval, the latter has a joint interval and fixed, there is compensation after the termination of the seizure Intermittent; 4 former without ventricular fusion wave and the latter; 5V1 ~ V6 lead QRS wave direction is consistent, both up or down, highly suggestive ventricular tachycardia; 6 such as continuous deformity QRS wave, such as the electric axis Most of the directional changes are ventricular tachycardia (torsional ventricular tachycardia).

Pre-excitation syndrome

The characteristics of ventricular tachycardia with atrial fibrillation and ventricular tachycardia are:

1 ventricular rate is 140 ~ 200 times / min, more than 180 times / min is rare; 2 ventricular rhythm can be slightly irregular or completely neat, RR interval is only 0.02 ~ 0.04s; 3QRS wave is rarely right bundle branch resistance The stagnation pattern, no pre-shock; 4 can be seen in the ventricular capture, there is a ventricular fusion wave; the electrocardiogram before and after the onset of 5-ventricular tachycardia can present the same form of ventricular premature contraction.

The characteristics of pre-excitation syndrome with atrial fibrillation are:

1 ventricular rate is more than 180 ~ 240 times / min; 2 ventricular rhythm is irregular, RR interval can be greater than 0.03 ~ 0.10s; 3QRS wave width deformity, but the pre-shock can be seen at the beginning; 4 without ventricular capture Therefore, there is no ventricular fusion wave; 5 before and after the attack, the electrocardiogram can be seen in the pattern of pre-excitation syndrome.

4. Identification of atrial fibrillation and atrioventricular junctional heart rhythm

In some cases, the f-wave of atrial fibrillation is so small that it cannot be clearly displayed on a conventional electrocardiogram. At this time, it is easy to be misdiagnosed as a ventricular tachycardia at the atrioventricular junction, but the ventricular rhythm is absolutely irregular during atrial fibrillation ( With third-degree atrioventricular block (except for), and the atrioventricular junctional heart rhythm is absolutely uniform. In addition, if the gain f wave can be increased, it can appear in special lead (such as esophageal lead). To the f wave, you can diagnose atrial fibrillation.

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