Cardiac Arrhythmia Cardiac Arrhythmia Definition Cardiac Arrhythmia Diagnosis Cardiac Arrhythmia Drugs Cardiac Arrhythmia Meaning Cardiac Arrhythmia Types Diagram. Heart Arrhythmia Images Illistration

Cardiac Arrhythmias Meaning Definition Symptoms Types and Drugs

Definition of cardiac Arrhythmia: Arrhythmia refers to any abnormality at the origin of the heart rhythm, heart rate and rhythm, and impulse conduction.


Meaning of Cardiac Arrhythmia (Cardiac origin conduction system)

Cardiac Arrhythmia Meaning: The cardiac pacing conduction system includes the sinoatrial node, the nodal node bundle, the atrioventricular node, the left and right bundle branches of the atrioventricular bundle (Hirst bundle), their branches and the Puqingye fiber network. The sinoatrial node is located at the entrance of the right superior atrial vena cava. It is the pacemaker to control the normal activity of the heart (also known as Heath bundle). The atrioventricular bundle first issues the left bundle branch after the branch, and then separates the left bundle branch before the branch, which itself continues into the right bundle branch, forming three systems. The posterior branch of the left bundle branch is slender and the branch is late. The two branches are branched under the endocardium and branch toward the apical branch. The thin branches kiss each other to form a net which is called Pujiye fiber net and penetrates into the ventricular muscle.


Cardiac conduction system

The blood supply of the cardiac conduction system, the sinoatrial node, the atrioventricular node and the trunk of the atrioventricular bundle are mostly supplied by the right coronary artery. The posterior branch of the left bundle branch is supplied by the left coronary artery and the right coronary artery.


Classification of heart arrhythmias

I. Classification of heart arrhythmias by Pathophysiology


(1) Arrhythmia due to abnormal origin of impulses

1. Sinus arrhythmia: Sinus tachycardia, Sinus bradycardia, Sinus arrhythmia, Sinus arrest and Sinus block.


2. Ectopic rhythm


(1) Passive ectopic heart rhythm:  

i. escape beat (atrial, atrioventricular junction, ventricular)

ii. escape beat rhythm (atrial, atrioventricular junction, ventricle).


(2) Active ectopic rhythm:

i. Premature beat (atrial, atrioventricular junction, ventricular)

ii. Paroxysmal tachycardia (superventricular, ventricular)

iii. Atrial flutter, atrial fibrillation

iv. Ventricular flutter, ventricular fibrillation


(2) Arrhythmia due to impulse conduction abnormalities


a. Physiological radon interference and atrioventricular separation.


b. Pathological iliac sinus atrial block, intraatrial block, atrioventricular block, intraventricular block (left, right bundle branch and left bundle branch block).


c. Atrioventricular conduction pathway abnormal pre-excitation syndrome.

Classification by clinical heart rate changes


Clinically, arrhythmia can be divided into two categories of rapidity and slowness according to the speed of the heart rate at the time of its onset. This classification method is simple and practical.


(A) tachyarrhythmia


1. Premature beats (atrial, atrioventricular junction, ventricular)


2. Tachycardia


(1) Sinus tachycardia


(2) supraventricular


Paroxysmal supraventricular tachycardia


Non-reentrant atrial tachycardia


Nonparoxysmal junction tachycardia


(3) Ventricular


Ventricular tachycardia (paroxysmal, persistent)


Tip twist type


Accelerated ventricular autonomic rhythm


3. Flutter and tremble


Atrial flutter, atrial fibrillation, ventricular flutter, ventricular fibrillation


4. Pre-excitation syndrome that can cause tachyarrhythmias


(B) Bradycardia


1. Sinus and bradycardia bradycardia, sinus arrest, sinoatrial block, sick sinus node syndrome


2. Atrioventricular junction rhythm


3. Ventricular autonomic rhythm


4. Conduction block that causes bradyarrhythmias


(1) AV block first degree, second degree (type I, type II) & third degree


(2) Intraventricular block complete right bundle branch block, complete left bundle branch block, left anterior branch block, left posterior branch block, bilateral bundle branch block, right bundle branch block Combined branch block and three branch block.


Mechanism of Arrhythmia

I. The Mechanism of Tachyarrhythmia

(A) Impulse conduction abnormality-reentry reentry is the most common mechanism of tachyarrhythmia. The conditions for forming reentry excitement are:

1. The electrophysiological heterogeneity of two or more parts of the heart (ie, the difference in conductivity or refractory), these parts are connected to each other to form a potential closed loop.

2. On the basis of the pathway, a unidirectional block occurs in a channel

3. The conduction of the conductive channel is slowed down, so that the initially blocked channel has time to recover its excitement

4. The re-excitation of the initially blocked channel can complete a reentry Excitement. Impulses cycle through this loop repeatedly, causing persistent arrhythmia. Reentrant arrhythmia can be initiated and terminated by premature beats, and can also be terminated by rapid stimulation (known as overspeed suppression). These characteristics help to distinguish reentrant arrhythmias from those caused by triggering activities.


(B) Increased autonomy. Increased autonomy in the sinoatrial node and ectopic pacemaker. The spontaneous removal of the sinoatrial node or some of its conductive fibers is extremely high, and the excitement formed there can control the entire heart and cause tachycardia. Or issue an impulse in advance to contract before the formation period. It usually occurs in the following pathophysiological states:

1. Endogenous or exogenous catecholamines increase

2. Electrolyte disorders (such as high calcium, hypokalemia)

3. Ischemia and hypoxia

4. Mechanical effects (such as enlarged heart)

5. Drugs such as digitalis.


(C) Triggered activity In some cases, such as increased local catecholamine concentration, hypokalemia, hypercalcemia, digitalis poisoning, etc., triggering can be seen in the atrium, ventricle or Heath-Purkinje tissue activity. These factors cause the accumulation of intracellular calcium and cause depolarization after action potentials, called post-depolarization. When the amplitude of the post-depolarization continues to increase, it can reach the threshold level and cause repeated excitement. Paroxysmal tachycardia can be formed by successively triggering stimuli.


Depolarization after action potential (ie, post-delay potential) amplitude



Reaching the threshold level, causing continuous triggering of excitement and formation of paroxysmal tachycardia


II. The Mechanism of Bradycardia

(1) Impaired autonomic dysfunction of sinoatrial node. For example, due to inflammation, ischemia, necrosis or fibrosis, sinus node failure, pacing dysfunction, sinus bradycardia and sinus arrest, etc.


(2) Conduction block sinoatrial node and atrial lesions can cause sinoatrial block, intra-atrial block.

Atrioventricular block is due to the reduction of the conduction function of the atrioventricular node or the atrioventricular bundle. Myocarditis, diphtheria and other infections, coronary heart disease, digitalis poisoning, etc., are mostly physiologically excitable. Atrioventricular block is divided into three degrees according to the degree.



Tachyarrhythmias include premature beats, paroxysmal tachycardia (supraventricular, ventricular), flutter and fibrillation (atrial, ventricular), and pre-excitation syndrome.



Premature beats are referable to as premature beats, and ectopic pacing points (atrial, ventricular, and atrioventricular node areas) other than the sinus node are caused by premature excitement. Excessive smoking, drinking, strong tea, emotional situation. Also, there can be induction of fever. Common in a variety of heart diseases such as coronary heart disease, acute myocarditis, cardiomyopathy and hyperthyroid heart disease, digitalis drugs, antimony, quinidine, chloroform and other toxic effects, hypokalemia and cardiac surgery or heart catheter examinations can be caused.


Clinical Manifestations of Pre mature Beats

1. Symptoms: Premature beats may be asymptomatic, and palpitations or palpitation may also be present. Frequent premature beats cause fatigue, dizziness and chest tightness when the cardiac output is reduced, and can exacerbate angina pectoris or heart failure.


2.  We can find physical signs and physical examination in the basic heart rhythm between the early pulse, followed by a longer interval. The heart sounds of atrial premature beats are similar to the basic rhythm. The first heart sound of atrial premature beats is mostly enhanced or reduced, the second heart sound is not audible. The radial artery pulse caused by premature beats is weak or unreachable, forming a leaky pulse, which is the result of ventricular filling and low blood volume. When the premature beats are in the triple or triple rhythm, you can hear a break after every 2 or 3 beats. Premature beats are inserted between two basic heartbeats called insertional premature beats. Auscultation can connect three beats that are faster than the basic heartbeat.


ECG Features

It can be divided into three types, atrioventricular, junction and atrioventricular. Among them, ventricle is the most common, followed by atrioventricular and junction.


1. The premature P wave of atrial premature beats is different from the P wave of sinus rhythm. The P-R interval is> 0.12 seconds. The QRS complex is mostly the same as the sinus rhythm, sometimes slightly widened or deformed, with the corresponding changes in ST segments and T waves. This is called indoor differential conduction. It needs to be distinguished from ventricular premature beats. The former QRS complex can be seen in front of P ‘waves The P-R interval is> 0.12 seconds, and the V1QRS complex is mostly rsR ‘. There is no QRS wave after the premature deformity P ‘wave, which is called atrial premature beat.


Preatrial contraction and preatrial contraction with differential indoor transmission.


2. The premature beat at the junction of the atrioventricular Premature QRS complexes, which have the same morphology as sinus or have indoor differential conduction. There are sometimes retrograde P waves before and after the QRS complex. The P’-R interval is shorter than 0.12 seconds, or there are no P ‘waves. The compensation period can be incomplete or complete.


3. Premature ventricular premature beats have QRS complexes that appear prematurely. Their morphological abnormalities are mostly ≥0.12 seconds. The T wave is opposite to the main wave of the QRS complex. The S-T segment shifts with the direction of the T wave and has no correlation before it. P wave, there is a complete compensatory interval (Figure 3-5). Ventricular premature beats can occur between two sinus beats, forming an intervening premature ventricular beat.


4. Atrial or ventricular premature beats are sometimes produced by more than two pacing points. The P wave of atrial premature beats and the QRS wave of ventricular premature beats in ECG have two or more different forms and are paired. Intervals vary and are called multi-source premature beats. Frequent premature beats can occur one after another. If more than 3 times, it is called short-term tachycardia.


5. The rhythm of premature beats with parallel rhythms is characterized by the non-constant pairing interval, but there is a fixed regularity between premature beats. The longest premature beat interval and the shortest premature beat interval have an integral multiple relationship. Atrial or ventricular fusion waves often appear.


Clinical Significance

Premature beats occur in the heart without organic lesions, and are mostly of no clinical significance. Frequent atrial premature beats, seen in mitral valve disease, hyperthyroidism, or coronary heart disease, especially multi-source, may be a prelude to atrial fibrillation. Ventricular premature beats that occur in the following situations may be ventricular tachycardia or the prelude to ventricular fibrillation should be highly valued and dealt with in a timely manner:

1.   Frequent (> 6 times / minute or 30 times / hour), which is continuous and consistent, and 2-3 premature beats occur continuously, showing multi-source or short array Patients with tachycardia; QRS complex abnormalities or time limit> 0.14 seconds.

  1.      Premature ventricular contractions within 72 hours of acute myocardial infarction.
  2.      Digitalis or antimony poisoning.
  3.      Premature ventricular contractions caused by hypokalemia.
  4.       Acute myocarditis.
  5.       Quinidine syncope, QT prolonged syndrome within 24 hours after extracorporeal circulation.


The pattern of ventricular premature beats can help diagnose myocardial infarction; for example, the QRS waveform of premature beats is wide and QR-shaped with ST segment elevation. Even if the myocardial infarction pattern in sinus rhythm is not obvious, the possibility of acute myocardial infarction should be considered.


Treatment of Ventricular Premature Beats

The main purpose of treating ventricular premature beats is to prevent ventricular tachycardia, ventricular fibrillation and sudden cardiac death. However, the causal relationship between premature ventricular death and sudden cardiac death has not been determined. Also, there is no evidence that antiarrhythmic drugs inhibit ventricular early prevention of sudden death. It must also be mentioned that antiarrhythmic drugs themselves can cause fatal arrhythmias. Therefore, the choice of antiarrhythmic drugs must be prudent.


1. For patients without heart disease, ventricular early does not increase its mortality. For asymptomatic isolated ventricular early, regardless of its shape and frequency, no medical treatment is needed. When symptoms occur, it should be explained to the patient first to reduce their anxiety. Use anti-arrhythmic drugs to reduce ventricular dysfunction early to reduce symptoms.


2. For the early ventricle associated with organic heart disease, the primary disease should be treated. When the exercise is taking place, or the continuous electrocardiogram monitoring shows that the short-term continuous ventricular early, or the early ventricular angina causes serious symptoms, you should treat the response room. For early treatment, premature ventricular contractions that require urgent treatment can be intravenously injected with 50-100 mg lidocaine until the premature beats disappear or the total amount reaches 250 mg. After arrhythmia is corrected, 1-3mg can be instilled every minute as needed. After stabilization, it can be changed to oral medication for maintenance. Lidocaine works within minutes after intravenous injection and lasts for 15-20 minutes. The therapeutic dose had little effect on myocardial contractility, blood pressure, and atrioventricular or intraventricular conduction. Side effects include dizziness and drowsiness. Large doses can cause convulsions, respiratory or cardiac arrest and can aggravate the original atrioventricular or intraventricular block. Use with caution in patients with liver and kidney dysfunction or severe heart failure.


3. Ventricular premature beats caused by digitalis poisoning In addition to drug withdrawal, intravenous phenytoin sodium or intravenous potassium chloride is often effective. For premature beats caused by hypokalemia, the cause should be actively removed to correct hypokalemia. Potassium supplementation is safer to take orally. Potassium citrate or potassium chloride is commonly used, 3-6g / day. When the condition is severe or can not be taken orally, potassium chloride is dripped intravenously. The commonly used concentration is 1000% 5% glucose solution. Potassium 20-30ml. The concentration of intravenous potassium supplement is preferably not more than 40mmol / L. It should not exceed 60mmol / L at most, and it should be infused intravenously evenly. Its rate should not exceed 20mmol per hour, and the total daily potassium supplementation should not exceed 200mmol. If a large amount of potassium supplementation is necessary in the short term, ECG monitoring and continuous observation of blood potassium should be performed. For those with an hourly urine output of less than 30ml, potassium supplementation should be done cautiously or temporarily.


4. Ventricular premature beats occurred during quinidine syncope or antimony treatment, quinidine or antimony should be discontinued. Oral drugs can be used:

i. Slow heart rate 0.1 ~ 0.2g, once every 8 hours. Excessive dose can cause Severe gastrointestinal reaction.

ii. β-blockers, such as propranolol 10-20mg, 3-4 times / day, those with heart failure or bronchial asthma are contraindicated.

iii. Digitalis; it is suitable for premature ventricular contraction caused by heart failure instead of digitalis poisoning. Digoxin 0.125mg is usually taken orally twice a day, and it is changed to once a day after a week.

iv. Procainamide 0.25g is taken orally once every 8 hours. After premature beat control, it is changed to 0.25-0.5g 3 times a day.

v. Amiodarone was taken orally 0.2 times, 3 times a day, and changed to 0.2 a week later. Diisopramine, Xinpingping, Antaxin, Changroline, Vencaine, Ethylzine and Incaramide are also available.


5. Atrial premature beats should be actively treated for the cause of the disease. Remove the inducement and choose the following drugs:

i. β adrenergic blockers, such as propranolol 10 ~ 20mg, 3 to 4 times per day orally.

ii. Isopadine 40 ~ 80mg, 3-4 times / day, the above two drugs are contraindicated for those with hypotension and heart failure.

iii. Digitalis, suitable for atrial premature beats caused by heart failure but not digitalis. Digoxin 0.25mg, 1 time / day.

iv. Quinidine can be tried 0.1g first, then 0.2g, orally 3-4 times a day.

v. Phenytoin sodium 0.1g, 3 times / day.

vi. Amiodarone 0.2g, 3 times / day, and then gradually decrease 0.1 ~ 0.2g, once / day. The treatment of atrioventricular junction premature beats is the same as that of atrioventricular premature beats. If it is not effective, drugs for treatment of ventricular premature beats can be tried.


Sinus tachycardia (Sinustachycardia)

The rate of sinus node impulses in adults is more than 100 times per minute, which is called sinus tachycardia, and the rate is usually between 101-160 times per minute. When sinus tachycardia begins and ends, its heart rate gradually increases and decreases.


Healthy people exercise and emotional stress can cause tachycardia. Alcohol, tea, coffee, and drugs such as isoproterenol and atropine often cause sinus tachycardia. Common causes in the disease state are fever, hypotension, hypoxia, cardiac insufficiency, anemia, hyperthyroidism, and myocarditis.


The ECG showed sinusoidal P waves with a P wave rate of more than 100 times per minute and a P-R interval greater than 0.12 seconds.


Treatment is mainly directed at the cause, and sedatives or beta-blockers can be used if necessary.


Paroxysmal Tachycardia

Paroxysmal tachycardia is a regular rhythm of paroxysmal tachycardia. It is characterized by sudden onset and sudden stop. According to the location of the ectopic pacemaker, it can be divided into atrial, nodular, and ventricular paroxysmal tachycardia. Atrial and nodular tachycardia are sometimes difficult to distinguish, often collectively referred to as supraventricular tachycardia.


Cause of paroxysmal supraventricular tachycardia

The cause of paroxysmal supraventricular tachycardia is the most common in Chinese people as pre-excitation syndrome (including occult sidewalks), accounting for about 60%, and atrioventricular node dual channels account for 30%. Other heart diseases include coronary heart disease, Idiopathic cardiomyopathy, hyperthyroidism, digitalis poisoning, etc. account for about 10%. Ventricular paroxysmal tachycardia is often accompanied by a variety of organic heart diseases, most commonly in coronary heart disease, acute myocardial infarction, mitral valve Prolapse, Ebbstein deformity, cardiac surgery, and prolonged QT interval syndrome can also be seen in idiopathic tachycardia in organic heart disease. Causes include exercise, excessive fatigue, emotional agitation, pregnancy, drinking or smoking.


Pathogenesis of paroxysmal supraventricular tachycardia

Electrophysiological studies have shown that reentry is the mechanism that causes most paroxysmal supraventricular tachycardia. Reentry can occur in the sinoatrial node, atrium, atrioventricular node, and major reentry pathways-including through the atrium The normal conduction of the nodule and the reentry of the atrioventricular by-pass in the atrioventricular node and by the occult by-pass with no preexcitation performance account for about 90% of paroxysmal supraventricular tachycardia.


The mechanism of atrioventricular node reentrant tachycardia: the dual channel of atrioventricular node is the basis of atrioventricular node reentry. This concept assumes that the AV node is longitudinally separated into two functionally different channels.

i. The beta channel conducts quickly but should not be long (fast channel)

ii. The alpha channel conducts slowly but should not be short (slow channel). Additional atrial stimulation can be blocked when the beta channel encounters its refractory period, and it is slowly conducted along the alpha channel. If the conduction of the alpha channel is slow, the original unresponsive beta channel gains time to recover excitability, the impulse can be reversed along the beta channel, forming a single atrial echo or continuous tachycardia. The maintenance of this reentry depends on the relative balance of conduction velocity and refractory period in the atrioventricular node. Because the depolarization of the atrium and ventricle occurs at the same time, the P wave on the surface electrocardiogram is not obvious.


Schematic diagram of reentry mechanism

The near-end common channel is divided into two scattered channels, α and β channels, and then merged into a common channel at the far end.

a. Under normal circumstances, conduction occurs simultaneously in the alpha and beta channels.

b. Premature beats encounter a unidirectional block in the beta channel, and conduction is delayed in the alpha channel.

c. The excitability of the beta channel has been restored, allowing the impulse to pass down the alpha channel to return to the beta channel to upload, causing reentry.

d. The reentry persists.


The reentry path of atrioventricular reentrant tachycardia is a combination of the normal atrioventricular conduction channel and the by-pass, and the atrioventricular by-pass only conducts in the retrograde direction. In this way, the impulse goes straight from the atrium along the atrioventricular node, the Heath-Urano system to the ventricle, and then returns to the atrium retrogradely through the hidden sidewalk. This arrhythmia is the same type as the preexcitation syndrome complicated by supraventricular tachycardia. But the former sidewalk does not conduct in the forward direction. Atrioventricular reentrant tachycardia can be initiated and terminated by the atrioventricular, as well as by the early ventricular.


The pathogenesis of ventricular paroxysmal tachycardia is mainly indoor microreentry, and a few are large bundle branch reentry. Ventricular ectopic pacing points have abnormally increased autonomic rhythms and triggering activities that account for only a few of tachycardia.


Clinical manifestations of Supraventricular paroxysmal tachycardia

Supraventricular paroxysmal tachycardia occurs suddenly and the heart rate increases to 150-250 beats per minute, which may last for seconds, hours or days. Palpitations may be the only symptoms, but if you have a heart attack or a heart rate of more than 200 beats per minute, you may show weakness, dizziness, angina, dyspnea, or fainting. If tachycardia occurs with typical angina. Or if there is an ischemic ST segment change, which persists until 1-2 weeks after the tachycardia stops, suggesting that coronary heart disease may be present. During the physical examination, the heart rhythm was regular, and the intensity of the first heart sound was consistent.


Ventricular paroxysmal tachycardia due to rapid heart rate and atrial contraction and ventricular contraction, resulting in reduced ventricular filling, reduced cardiac output, and hemodynamic abnormalities. Its severity depends on the basic condition of the heart and the duration of tachycardia. Dyspnea, angina, hypotension, oliguria, and fainting can occur. When this happens in an acute myocardial infarction, it may indicate that ventricular fibrillation may be imminent. At the time of auscultation, the first and second heart sounds split widened, the heart rhythm is basic or slightly irregular, and the first heart sound intensity is inconsistent.



I. Paroxysmal atrial tachycardia:

i. Continued rapid and regular heartbeat for more than 3 times, the P wave morphology is abnormal

ii. P-R interval> 0.12s

iii. QRS wave group morphology and sinus.

iv. Atrial rate is 160-220 times per minute.

v. Sometimes the P wave is superimposed on the T wave of the previous heart beat and is difficult to recognize. May be accompanied by first or second degree AV block.


II. Paroxysmal junction tachycardia

1.   Premature beats in the atrioventricular junction zone 3 consecutive times or more, with a frequency of 160-250 beats per minute, rhythm.

2.   The shape of P ‘wave and QRS complex has the characteristics of the aforementioned premature beats at the junction of the atrioventricular junction, and P’ wave can be retrograde before, during or after the QRS complex. It may be accompanied by different degrees of forward or reverse conduction block, and atrioventricular separation may occur at the same time or at different times.


If atrial and junctional tachycardia cannot be distinguished, they can be collectively referred to as supraventricular paroxysmal tachycardia.


Supraventricular tachycardia (connected to the upper) compresses the carotid sinus to stop the attack



III. Paroxysmal ventricular tachycardia

1.   More than 3 consecutive rapid premature ventricular beats, QRS complex deformity, time ≥ 0.12 seconds, the frequency is regular or slightly irregular.

2.   Sinusoidal P waves have nothing to do with QRS, showing atrioventricular separation. The frequency of P waves is slow, and it is difficult to find them because they are buried in the QRS complex.

3.   Sometimes see ventricular capture and ventricular fusion wave. The shape of the QRS complex captured by the ventricle is close to normal, with occasional retrograde conduction of the 1: 1 atrioventricular, P ‘waves follow the QRS complex, and at the same time, they have various degrees of atrioventricular block.


Ventricular paroxysmal tachycardia

Differential Diagnosis for Paroxysmal supraventricular tachycardia

Paroxysmal supraventricular tachycardia with differential conduction in the room should be distinguished from paroxysmal ventricular tachycardia.


Items paroxysmal ventricular tachycardia paroxysmal supraventricular tachycardia

Frequency Rarely> 200 times / minute Mostly 160-200 times / minute

Rhythm Relative Rule Very Regular

V1 is rsR ‘Rare Common

Ventricular capture yes yes no

Ventricular fusion wave yes no

Room rate / Room rate < 1 = 1

Compression of carotid sinus without change in ventricular rate


Treatment of Paroxysmal supraventricular tachycardia


I. Supraventricular paroxysmal tachycardia


(A) Treatment of acute attacks: Those with persistent attacks or organic heart disease should control their attacks as soon as possible.


1. Remove the cause

2. Stimulation of the vagus nerve

       i.  Use tongue depressor to stimulate uvula and induce nausea and vomiting.

ii.               Exhale deeply after inhaling, and then forcefully exhale (Valsalva method) or exhale deeply, and then inhale strongly (Muller method).

iii.            Carotid sinus massage: Listen to the carotid artery before the massage. The patient took a supine position to avoid syncope. First massage the right side for about 10 minutes. If it does not work, massage the left side. Do not massage both sides at the same time to avoid causing cerebral ischemia. At the same time as carotid sinus massage, Valsalva may improve the effect. If medication alone is not effective, carotid sinus massage can be used to stop tachycardia.

iv.             Squeeze the eyeball: The patient takes a supine position, closes the eyes and looks down. Use the thumb to press the upper part of the eyeball moderately under one side of the orbit for 10 seconds each time. Pressing the eyeball can cause retinal detachment.


3.Drug Treatment

i. Isoptin: Patients with no heart failure are the first choice. Generally, they are slowly injected intravenously after dilution with 5 mg, and the supraventricular tachycardia is not terminated, and then 5 mg is given, and the total amount is generally not more than 15 mg.

ii. Cedipandil: For those with large heart, especially those with heart failure, if digitalis-free drugs are not used within two weeks, it is preferred to inject 0.4mg of cedilan for intravenous injection, which is invalid after 2 hours, and then 0.2mg for 24 hours. The total amount does not exceed 1.2mg.

iii. Booster drugs; by raising blood pressure to stimulate the vagus nerve reflexively to achieve the purpose of terminating supraventricular tachycardia. Can be used phenylephrine 0.5-1mg or 10-20mg dilution of methamphetamine intravenous slow bolus or rapid infusion, the systolic blood pressure does not exceed 21.3 ~ 24.0kpa (160-180mmHg) as the degree. Once tachycardia has stopped, the drug should be discontinued. Not suitable for patients with organic heart disease or hypertension.

iv. 10-20mg of adenosine triphosphate (ATP) is added to the intravenous injection after dilution. Patients with sick sinus syndrome are contraindicated.

v. Neostigmine: For vagus nerve stimulation, use 0.5-1mg subcutaneously or intramuscularly; those with organic heart disease or bronchial asthma are contraindicated, often causing abdominal pain or hyperactive bowel sounds, this drug is generally less commonly used.

vi. It can also be intravenously injected or infused after being diluted with amiodarone or Xinpingping. Quinidine, procainamide, etc. are taken orally. Through the induction of electrophysiological examination and observation of drug tests, to select more sensitive and effective drug treatment.


4. Synchronous DC cardioversion: When the above methods are ineffective, synchronous DC cardioversion can be considered. However, those with tachycardia and hypokalemia caused by digitalis poisoning should not be treated with cardioversion.


5. Individuals with conditions can use esophagus or direct cardiac pacing alone or in combination with drugs, and stop tachycardia with super-speed stimulation or burst burst stimulation.


6. Those with frequent attacks and ineffective drug treatment prevention may consider performing endocardial catheter ablation, radiofrequency or surgery to block the reentry path based on electrophysiological mapping.


(B) For patients with frequent recurrence and seizures, oral medications that can control the seizure can be used, such as verapamil, Xinpingping, or amiodarone during oral administration. And should avoid the causes of seizures.


Ventricular paroxysmal tachycardia

(1) Treatment of acute episodes Ventricular paroxysmal tachycardia can cause severe hemodynamic disorders and can even develop into ventricular fibrillation, which must be addressed.


1. Treatment incentives and primary disease


2. For drug treatment, lidocaine 50-100mg is preferred. After dilution, it is slowly and intravenously injected. After it is effective, it is maintained at 1-4mg / min. Also available 150-300mg of amiodarone dissolved in 250ml of 10% glucose solution intravenously. Can also choose procainamide, amprolidine, diisopropylpyridine, and equal heart rate. In cases of digitalis poisoning, 150-250 mg of phenytoin sodium is dissolved in 20 ml of water for injection, and it is slowly and intravenously administered. It is necessary to give 100 mg after 5-10 minutes. Ventricular tachycardia occurs on the basis of high AV block or sick sinus node syndrome. Isoprenaline should be used 0.5mg%, intravenous drip.


3. Those with conditions can use esophagus or direct cardiac pacing alone or in combination with drugs, and use procedures to stimulate tachycardia or short burst stimulation to terminate tachycardia.


4. Electric therapy Synchronous direct current cardioversion; in critical condition, synchronous direct current cardioversion should be applied immediately after 1-2 doses of lidocaine are ineffective. ② Refractory ventricular tachycardia can be ablated with DC or RF catheter.


(2) Prevention of recurrence After the onset of seizures is stopped, drugs that can control the seizure can be taken orally to prevent recurrence.

Atrial flutter and atrial fibrillation


Atrial flutter and atrial fibrillation are arrhythmias that occur in the atrium and have a higher impulse frequency than atrial tachycardia. When the frequency of atrial ectopic pacing points reaches 250-350 beats / min, the atrial contraction is rapid and coordinated as atrial flutter. If the frequency is> 350 beats per minute and irregular, it is atrial fibrillation. Both can have both paroxysmal and chronic persistent types.




The causes of atrial flutter and fibrillation are basically the same. The most common are rheumatic heart disease, mitral valve stenosis, coronary heart disease, hyperthyroid heart disease, cardiomyopathy (including Keshan disease), myocarditis, and hypertensive heart disease. . Others include constrictive pericarditis and sick sinus node syndrome. A few cases of paroxysmal atrial fibrillation have no obvious cause, and they are called idiopathic atrial fibrillation. In recent years, some people think that it may be related to factors such as viral infection or degeneration of conductive tissues or instability of autonomic nerves.




The pathogenesis of atrial flutter and fibrillation: mainly the reentry agitation and ectopic pacemaker increase in autonomy, but the theory of multiple or micro-reentry agitation is more reasonable.


[Clinical manifestations]


The effect on hemodynamics and cardiac function and the symptoms it causes mainly depend on the recovery of ventricular rate and the severity of the original heart disease. The ventricular rate is often faster during the onset of a burst or persistent onset, and symptoms such as palpitations, chest tightness, and panic are more pronounced. Ventricular rate closer to normal has less effect on circulatory function and the symptoms are milder. Rapid atrial fibrillation, acute elevation of left atrial pressure and pulmonary venous pressure can cause acute pulmonary edema. Atrial fibrillation is also prone to cause thrombosis in the atrium, and part of the thrombus can cause systemic arterial embolism.


The main signs of atrial fibrillation are absolutely irregular heart rhythms and varying heart sounds. The patient’s pulse rate is significantly less than the heart rate, which is called short pulse basis. The arrhythmia may be regular or irregular, depending on the ratio of atrial and ventricular conduction, such as 3: 1 or 6: 1. Ventricular rules.




1. Atrial flutter:

i. P wave disappears, and the shape, spacing, and amplitude are replaced by absolute rules. The atrial flutter wave (F wave) is sawtooth-like. The frequency is 250-350 times per minute.

ii. The most common atrioventricular conduction ratio is 2: 1, which produces fast and regular ventricular rhythms at about 150 times per minute, followed by the 4: 1 atrioventricular conduction ratio, forming a ventricular rate of 70-80 times per minute. Sometimes the atrioventricular conduction ratio is not constant, causing irregular ventricular rhythms.

iii. The shape of QRS complex is mostly the same as that of sinus rhythm, and it can also have differential conduction in the ventricle. (Figure 3-3-10)


Atrial flutter


Figure 3-3-10 Atrial flutter


2. Atrial fibrillation:

i. P wave disappears and is replaced by atrial fibrillation wave (f wave) with absolutely irregular shape, interval and amplitude, frequency 350-600 times per minute.

ii. QRS wave group interval is absolutely irregular, its shape and amplitude can be constant There are ranging. (Figure 3-3-11)


Atrial fibrillation




Atrial flutter and atrial fibrillation, in addition to the treatment of the etiology and inducement, attention should be paid to the control of ventricular rate, ectopic rhythm reversion and prevention of recurrence.


First, the atrial flutter when the ventricular rate is fast, should be treated with digitalis. In general, cedilan should be injected intravenously to control the ventricular rate below 100 times per minute. If atrial flutter persists, synchronous DC or quinidine reversion should be considered. The success rate of atrial flutter recovery rate is more than 95%, and the required electrical energy is small, which is safer than using quinidine, and it should be used first when conditions permit. Oral quinidine or amiodarone may also stop its onset. Repeatedly, the author needs to take quinidine or amiodarone for a long time to prevent it.


Atrial fibrillation


(A) Atrial fibrillation should first be treated for the primary disease. The ventricular rate is fast and the symptoms are obvious. Intravenous injection of cedilan is preferred to slow down the ventricular rate. In some patients, cedilan can be converted to sinus rhythm. If the symptoms are still severe, electrocardioversion can be used. In the absence of severe cardiovascular damage, digitalis, calcium channel blockers, or beta blockers can be used to extend the refractory period of the atrioventricular node, slow the atrioventricular conduction, and often effectively reduce the ventricular rate.


(2) Chronic atrial fibrillation Atrial fibrillation significantly reduces cardiac output, and if it can be converted into sinus rhythm, it is beneficial to the patient. However, both cardioversion and drug cardioversion have certain risks, and after cardioversion, they must be taken for a long time to maintain, and the recurrence rate is high. Therefore, when considering cardioversion, it is necessary to estimate the success rate of cardioversion and the possibility of maintaining sinus rhythm according to the specific circumstances of the patient, and weigh the advantages and disadvantages to make a decision.


After cardioversion, quinidine or similar drugs can be used to prevent recurrence. If cardioversion is unsuccessful or atrial fibrillation recurs, use a calcium antagonist, beta blocker, or digitalis to control ventricular rate.

Ventricular flutter and ventricular fibrillation (Ventriculer Flutter and Ventriculer Fibrillation)


Is the most serious arrhythmia. During ventricular flutter, the ventricle has fast and weak ineffective contractions; when ventricular fibrillation occurs, the muscle fibers in each part of the ventricle undergo faster and uncoordinated tremor, and both have an impact on hemodynamics equal to ventricular arrest.


Etiology and Pathogenesis 

Common acute myocardial infarction, severe hypokalemia, toxic effects of drugs such as digitalis, quinidine, chloroquine, etc .; cardiac surgery, low temperature anesthesia with electric shock and so on.


The pathogenesis is similar to atrial flutter and fibrillation.


Clinical manifestations 

Ventricular flutter and tremor, once it occurs, the patient immediately develops cardio-cerebral ischemia syndrome (Adrms-Stokes syndrome). This is manifested by loss of consciousness, convulsions, followed by respiratory arrest. No heart sounds or pulses were heard during the examination.



Ventricular flutter appears as regular and wide ventricular waves, with up and down amplitudes ranging from 150 to 250 beats per minute. Ventricular fibrillation is completely irregular in shape, frequency and amplitude, with a frequency of 150-500 times per minute.


Ventricular flutter



Ventricular fibrillation 

In the figure, irregular waves with different shapes and amplitudes can be seen. The frequency is about 320 / min. It is difficult to distinguish between QRS and T waves.



Cardiopulmonary resuscitation should be carried out immediately on the spot. The patient should lie supine with his head down and use the palm root to box 2-3 times at the lower end of the sternum in the anterior region of the heart, followed by external chest compressions and mouth-to-mouth and artificial respiration. Establish effective breathing channels, intravenous infusion channels, ECG monitoring, intravenous epinephrine, add atropine and lidocaine if necessary, and use some other drugs. Those who fail will be given electric shock defibrillation and cardiac pacing, and given corrective acid imbalance with electrolyte balance, hypoxemia, and other treatment measures. For high-risk patients who are prone to ventricular fibrillation and drug prevention is ineffective, an automatic defibrillator can be placed.


Pre-excitation Syndrome


[Classification and pathogenesis]


The atrial impulse causes the entire ventricle or a part of the ventricle to be excited in advance, or the ventricular impulse causes the entire atrium or a part of the atrium to be excited in advance, which is called pre-excitation syndrome. The most common type of pre-excitation is ventricular pre-excitation with accessory atrinventricular pathways (kent bundles). These by-passes consist of atrial muscle-like muscle bundles and can be found almost anywhere around the atrioventricular ring. The term Wolff-Parkiason-White syndrome (W.P.w syndrome) applies to patients with preexcitation on the ECG and paroxysmal tachycardia.


In addition, there are three abnormal channels. Atrioventricular node tract, that is, James fiber connects the atrium and the lower part of the atrioventricular node or the Heath bundle, such as the Down-Ganong-Levine syndrome. Two types of Mahaim fibers, including the fibers from the atrioventricular to the ventricle, are called nodal fibers, and the fibers originating from the Heath bundle or bundle branch, and the fibers attached to the ventricular muscle are called branch ventricular fibers. The PR interval may be normal when the nodules connect Or shortened, and the QRS complex is a fusion wave, the branch chamber connection produces a normal PR interval and a fixed abnormal QRS complex.



Anatomy classification of prepayment syndrome


Clinical Manifestations

Pre-excitation itself does not cause symptoms, but often leads to the onset of tachyarrhythmia. The occurrence of supraventricular paroxysmal tachycardia is similar to that of general paroxysmal supraventricular tachycardia. When atrial fibrillation or atrial flutter occurs, the ventricular rate can be as fast as 220-360 times per minute, leading to shock, heart failure, and even sudden death.












Chronic sinus arrhythmia

Chronic sinus arrhythmias include: sinus bradycardia, sinus arrest, sinoatrial block, and sick sinus node syndrome.

Sinus bradycardia (SinusBradycardia)


Sinus rhythm is slower than 60 beats per minute and is called sinus brady-cardia. Common in healthy adults, especially athletes, the elderly, and when sleeping. Other causes are increased intracranial pressure, hyperkalemia, hypothyroidism, hypothermia, and the use of digitalis, beta blockers, and reserpine. , Acetamidine, methyldopa and other drugs. In organic heart disease, sinus bradycardia can be seen in coronary heart disease, acute myocardial infarction (especially in the early stages of inferior myocardial infarction), myocarditis, cardiomyopathy, and sick sinus syndrome.


[ECG] is sinus rhythm, the heart rate is less than 60 times per minute, often accompanied by sinus arrhythmia.



If the heart rate is not less than 50 times per minute, it generally does not cause symptoms and does not require treatment. If the heart rate is below 40 beats per minute with angina pectoris, cardiac insufficiency or central nervous system dysfunction, atropine, ephedrine or isoproterenol can be used to increase the heart rate.


Sinus Arrest 

Sinus arrest means that the sinoatrial node does not produce impulses during one or more cardiac cycles so that it cannot excite the atria or the entire heart. Sinus arrest is often the result of inferior sinus node function. It can be seen in the toxic effects of digitalis and quinidine and sick sinus syndrome caused by various etiologies, and occasionally in patients with increased vagal tone.



It shows that the P wave is not seen for a significantly longer period of time than the normal P-P interval, or neither P wave nor QRS wave appears, but between the long P-P interval and the basic sinus P-P interval No common multiple relationship. Nodular or ventricular escape may occur after a long interval. If sinus arrest is too long, nodular or ventricular autonomic rhythms may occur. If the atrioventricular junction or ventricle fails to send impulses in time, the patient may have dizziness, and even fainting and convulsions, which is Adams-stodes syndrome.


Sinus arrest and borderline escape


Sinus arrest and borderline escape



Frequent sinus arrest and symptoms may be treated with atropine, ephedrine or isoprenaline. Patients with Adams-stokes syndrome should use isoproterenol 0.5-1mg in 500ml glucose solution intravenously. If the effect is not satisfactory or long-term infusion of isoproterenol should be considered, the device should be used for artificial cardiac pacing Device.


Sinoatrial Block 

Sinus block refers to the impulses generated by the sinoatrial node, some or all of which cannot reach the atrium, causing atrial and ventricular arrest. Transient sinoatrial block is seen in acute myocardial infarction, acute myocarditis, hyperkalemia, digitalis or quinidine effects, and hypervagal tone. The etiology of chronic sinoatrial block is often unknown, and it is more common in the elderly. The basic lesion may be idiopathic sinoatrial degeneration. Other common causes are coronary heart disease and cardiomyopathy. Sinus block can be divided into first degree, second degree and third degree according to the degree of block. However, only a second-degree sinoatrial block can be diagnosed from the ECG. The electrocardiogram showed long pauses between P waves. Is a multiple of the basic P-P interval. Sinus arrest does not have such a multiple relationship, which can be used for differential diagnosis. Wenckebach phenomenon can be seen in some cases. It is similar to the Venturi phenomenon in the second-degree atrioventricular block, but it shows a progressive shortening of the P-P interval instead of the R-R interval until a long interval occurs. Nodular escape may occur after sinoatrial block. In many cases, the interval before escape is quite long, suggesting that there is also an opportunity for low pacing points.


The clinical manifestations, significance and treatment of sinus atrial block are similar to those of sick sinus syndrome.


Venturi phenomenon of second degree sinoatrial block


Wen’s phenomenon of second degree sinoatrial block

Sick Sinus Syndrome (SSS)


Sick sinus syndrome is referred to as sick sinus syndrome. It is a complex symptom of a variety of arrhythmias and symptoms caused by sinus node atrial impulse formation, or sinus node to atrial impulse conduction disorder due to the original organic lesions of the sinoatrial node or surrounding tissue. The main feature is sinus bradycardia, which is called bradycardia-tachycardia syndrome when recurrent tachyarrhythmia occurs.


Cause and Pathology

Idiopathic sclerosis-degenerative changes, coronary heart disease, cardiomyopathy, myocarditis, rheumatic heart disease, surgical injury, hypertension, etc. Some are familial or unknown. The pathological changes are mainly sinoatrial node and atrial fibrous hyperplasia, which may be accompanied by occlusion of the sinoatrial node artery within the nodule, and may occasionally involve the atrioventricular junction and branches.


Clinical manifestations

Onset is insidious, progress is slow, and sometimes accidentally discovered. Symptoms such as inadequate blood supply to the heart, brain, gastrointestinal tract and kidneys, such as fatigue, chest pain, palpitations, dizziness, insomnia, memory loss, irritability, sluggish response, polyuria, and poor appetite. Can be persistent or intermittent. When a high degree sinus block or sinus arrest occurs, short-term syncope or dark haze can occur. Occasionally angina, heart failure or shock can occur. Acute inferior myocardial infarction and myocarditis can cause temporary sinus node dysfunction, which usually disappears after the acute phase.



In addition to clinical symptoms, the diagnosis should be further confirmed based on the following tests.


I. The electrocardiogram

i. Severe sinus bradycardia, less than 50 times per minute.

ii. Sinus arrest and / or sinoatrial block.

iii. Bradycardia and tachycardia appear alternately. Bradycardia is sinus bradycardia, tachycardia is supraventricular tachycardia, atrial fibrillation or flutter.

iv. Chronic atrial fibrillation cannot be converted to sinus rhythm after cardioversion.

v. Persistent and slow atrioventricular junction rhythm, some patients may be combined with atrioventricular block and bundle branch block.


II. Measurement of sinoatrial node function

The following methods can be selected for suspected patients:

(A) Exercise and atropine test Exercise or intravenous atropine 1.5 ~ 2mg, continuous observation of electrocardiogram or oscillography at 1, 2, 3, 5, 10, 15, 20 minutes after injection, such as sinus rhythm cannot be increased to 90 Times / minutes and / or positive sinus atrial block, junctional rhythm, and supraventricular tachycardia were positive. Such as sinus rhythm increase> 90 times / minus negative, mostly for hypervagus function, with caution in patients with glaucoma or obvious prostate hypertrophy.


(B) Detection of sinus node function by transesophageal or direct atrial pacing: This method is a more reliable diagnostic method for diseased sinus syndrome, especially combined with the effects of drugs blocking the autonomic nervous system, which can increase sensitivity. A bipolar pacing catheter is inserted through the esophagus, the electrodes are placed behind the left atrium, and then an artificial cardiac pacemaker is used for rapid pacing. The frequency has gradually increased from 90, 100, and 120 times per minute to 150 times per minute. Each pacing lasted 1 minute, then stopped pacing, and recorded the electrocardiogram to see how long the sinoatrial node can wake up and rebound. The time from the stop of pacing to the recovery of sinus P waves is the sinus node recovery. time. Patients with diseased sinus syndrome have an intrinsic heart rate below 80 beats / min (measured after atropine 2mg plus propranolol 5mg intravenously), sinus node recovery time> 1500m.s, and sinoatrial conduction time> 180m.s.


(C) Dynamic ECG monitoring: we can learn the fastest and slowest heart rate, sinus arrest, sinoatrial block and other arrhythmia.


(D) Exercise test: When treadmill or treadmill exercise test, if the heart rate does not increase significantly after exercise, it indicates that the sinus node function is poor. But must be closely monitored to prevent accidents.


Differential Diagnosis

First of all, we must exclude various factors that increase the excitability of the vagus nerve. After a detailed medical history, if the heart rate is slower than 60 beats / min at rest or at night, and the heart rate can reach 90 beats / min or more after activity or a little medication, it is considered physiological Bradycardia, suspicious persons can use auxiliary diagnostic methods to determine sinus node function.



1. The cause of treatment First, the etiology should be as clear as possible, such as coronary stenosis can be percutaneous coronary angioplasty, application of nitroglycerin and so on to improve coronary blood supply. Myocarditis can be treated with energy mixture, high-dose vitamin C intravenously or intravenously.


2. Drug treatment: For patients without tachyarrhythmia, try atropine, ephedrine or isoprenaline to increase heart rate. 600-1000mg of nicotinamide dissolved in 250-500ml of 10% glucose solution intravenously once a day to avoid the use of drugs that slow heart rate, such as beta blockers and calcium antagonists.


Traditional Chinese medicine treatment is mainly based on tonifying qi, warming the sun and promoting blood circulation. People can participate in moxibustion and licorice decoction, Shengmai San plus Sini decoction.


3. Install on-demand artificial cardiac pacemaker. It is best to choose atrial pacing (AAI) or frequency response pacemaker. On this basis, antiarrhythmic drugs are used to control tachyarrhythmia.


Escape Beat and Escape Rhythms 

Escape beat is the heartbeat caused by the pulsation of ectopic pacing points after the basic heartbeat is delayed or blocked. The most common site is the atrioventricular junction, but it can also occur in the ventricle or atrium. Successive escapes are called escape beat rhythms.



Commonly occurs when the sinoatrial node is autonomically decreased or the sinoatrial or atrioventricular block is more than degree. It is also seen in increased vagal tone, sick sinus node syndrome, anesthesia, digitalis and quinidine drug poisoning, coronary heart disease, Cardiomyopathy and myocarditis.



Junction zone escape beat rhythm is the junction escape beat for 3 consecutive times. The heart rate is slow and regular, with 40-60 beats per minute, P waves are not seen or present at the junction zone, that is, inverted in lead II, III, avF, and upright in AvF. The shape of QRS complex is the same as that of sinus. The P wave may be before, during, or after the QRS complex. (Figure 3-3-18)


Escape rhythm 

The clinical significance of junctional zone rhythm depends on its etiology. Transient seizures are associated with increased vagal tone and are mostly insignificant. Persistent seizures may indicate an organic heart disease or a drug-induced sinus node dysfunction or atrioventricular conduction disorder.


Ventricular autonomic rhythm is an ectopic escape rhythm that originates from the ventricle. The heart rate is 30-40 times per minute. It is found in the sinoatrial node or the interface between the atrium and the atrioventricular tissue in a state of inhibition or third degree atrioventricular conduction below the branch of the atrioventricular bundle When blocked, it can also be caused by poisoning with quinidine and other drugs, and it is often a heart rhythm before death. The electrocardiogram shows that the ventricular rhythm is regular or irregular, and the QRS complex is wide and deformed (the deformity originating from the proximal end of the bundle branch may not be obvious). Ventricular autonomic rhythm before dying, QRS time limit can reach more than 0.16 seconds, and has a variety of forms, slow and regular ventricular rate. Ventricular autonomic rhythm can seriously affect cardiac output, causing hypotension, shock or Adms-Stokes syndrome.



Evasion itself is a protective physiological phenomenon, and should be treated according to the etiology and arrhythmia that cause it. Emergency symptomatic treatment of ventricular spontaneous heart rhythm can be intravenous infusion of isoproterenol.

Atrioventricular Block (Atrioventricular Block)


Atrioventricular block refers to the block of impulse during atrioventricular conduction. Divided into two categories of incompleteness and completeness. The former includes first-degree and second-degree atrioventricular block, and the latter is also called third-degree atrioventricular block. The block can be located in the atrium, atrioventricular node, Heath bundle and double bundle branch.



i. The cause of myocardial inflammation is most common for various reasons, such as rheumatic, viral myocarditis and other infections.

ii. The vagus nerve is excited, often manifested as transient atrioventricular block.

iii. Drugs: such as digitalis and other antiarrhythmic drugs, most of the discontinuation of the atrioventricular block disappeared.

iv. Various organic heart diseases such as coronary heart disease, rheumatic heart disease and cardiomyopathy.

v. Hyperkalemia, uremia and so on.

vi. Idiopathic conduction system fibrosis, degeneration and so on.

vii. Traumatic injury, accidental injury during cardiac surgery, or atrium conduction tissue can cause atrioventricular block.


Clinical Manifestations

Patients with first-degree atrioventricular block are often asymptomatic. At the time of auscultation, the first heart sound of the apex weakened, which was due to the prolonged P-R interval and the closeness of the atrioventricular leaflets at the beginning of ventricular contraction. Patients with second-degree type I atrioventricular block may feel asystole. Arrhythmia occurred during auscultation, and the first heart sound intensity may change with the change of P-R interval. Patients with second-degree type II atrioventricular block often have fatigue, dizziness, fainting, convulsions, and cardiac insufficiency, and often develop complete atrioventricular block in a short period of time. The arrhythmia at auscultation depends on changes in the atrioventricular conduction ratio. Symptoms of complete atrioventricular block depend on whether ventricular autonomic rhythm is established and the basic conditions of ventricular rate and myocardium. Ventricular arrest occurs if the ventricular autonomic rhythm is not established in time. The autonomic rhythm point is higher, such as just below the Heath bundle, the ventricular rate is as fast as 40-60 beats per minute, and the patient may be asymptomatic. Ventricular autonomic rhythm is very low in patients with double bundle branch disease, and the ventricular rate is slow below 40 beats per minute. Cardiac dysfunction and cerebral ischemia syndrome (Adams-Stokes, Syndrome) or sudden death may occur. Slow ventricular rate often causes increased systolic blood pressure and widened pulse pressure. Increased stroke volume produces jet murmurs and third heart sounds in the systole of the pulmonary valve area. Atrioventricular separation and atrioventricular contraction are not coordinated, resulting in irregular atrial sounds and loud first heart sounds.



Clinical application of commonly used antiarrhythmic drugs


In the past ten years, the treatment of arrhythmia has made great progress, including etiology treatment, drug treatment, electrical treatment and surgical treatment. The application of antiarrhythmic drugs is still the most important therapy.


First, antiarrhythmic drugs and their classification 

The commonly used is the modified Vaughan williams classification (1984), which is divided into four categories according to cell electrophysiology and clinical application, and class I is divided into three subclasses.


Class I: membrane inhibitors. It mainly reduces the permeability of myocardial cells to sodium ions, which reduces the rate and amplitude of myocardial action potential phase 0 rise, thereby slowing conduction, reducing membrane reactivity, extending the effective refractory period, and reducing The slope, which reduces self-discipline, is divided into three sub-categories.


Type IA: quinidine, procainamide, diisopropylpyramine, amprolidine, an azozoline, Manmailing, Pirmenol, and Cibenyoline.


Type IB: lidocaine, bradycardia, ventricular ancaine, phenytoin, ethmazine.


Class C: Incaramide, flucaramine, lavocamide, heart rate and Indecainide.


Table 3-2-3-2 Electrophysiological effects and ECG changes of Class drugs


Sub-type Inhibit O phase APD ERP ERP / APD Decrease conduction speed P-R QRS Q-T

A ↑↑ (↑ Q-T) ↑↑ ↑ ↑ (↑ HV) 0 ↑ 0 ↑ ↑↑↑

B weak ↓ (Q-T) ↓ ↑ small 0 - 0 ↓

C Strong ↓ ↑ ↑ ↑↑ (↑ HV) ↑ ↑↑ ↑


Type II: β-adrenergic receptor blockers, whose main role is to block or reduce the excitatory effect of sympathetic nerves on the heart muscle, including propranolol. Glycine reassurance, Mido reassurance, and equal experience.


Type III: Action potential extender. Prolong the action potential time and effective refractory period of cardiomyocytes, including amiodarone, bromobenzylamine, sotolol and so on.


Type IV: Calcium antagonists. Inhibiting the slow channel of calcium in myocardial cells and preventing the influx of calcium ions mainly affect the slow response fibers. Including isopidine, thiazezone.


Other drugs: including adenosine (adenosine), adenosine triphosphate, digitalis, potassium salts, isoprenaline and so on.


The above are only divided according to the main electrophysiological effects, and some drugs can have multiple electrophysiological effects. For example, amiodarone not only has a type III effect, but also has a type I sodium channel blocking effect. Amine and mesulfasalazine belong to the third class of drugs and also have the effect of class II drugs.

Second, commonly used antiarrhythmic drugs


(1) Quinidine is used for various cardioversion of premature beats, tachycardia, atrial fibrillation, and atrial flutter. At present, it is mainly used for the treatment of atrial fibrillation, atrial flutter cardioversion, and maintenance of sinus rhythm after electrical cardioversion. Sometimes it is also used for some refractory supraventricular or ventricular tachyarrhythmias that are difficult to control with other drugs. Cardioversion of atrial fibrillation should be taken orally once every 2 hours for a total of 5 times. If the dose is gradually increased, the dose of 0.1 g is gradually increased. Generally, a maximum of 0.4 g is used every two hours to avoid serious side effects. This drug has significant effects, but has a small safety range. The main problem is the occurrence of quinidine syncope, which is caused by ventricular tachycardia or ventricular fibrillation. Most scholars believe that its occurrence seems to be independent of dose, it can also occur at low doses, and may be associated with low potassium , Poor heart function, sensitivity to this drug and other factors.


(2) Procainamide is effective for both supraventricular and ventricular arrhythmias, and is mainly used for refractory ventricular tachycardia and pre-excitation syndrome combined with atrial fibrillation. Intravenous injection of 0.1 g plus 5% glucose in 20 ml slowly bolus for 5 minutes, 5 to 10 minutes once injection, the total amount does not exceed 1 g; also intravenous drip. It should be performed under ECG monitoring and close monitoring of blood pressure. Use caution when applying. Sometimes it is also used for the treatment of refractory ventricular early. The dosage is 0.25 to 0.5 grams 4 times a day, but it should not be maintained for a long time. Lupus syndrome occurs in nearly a third of cases after a few months of medication.


(3) Disopyramide

This has a similar effect to quinidine, and can be used for ventricular and supraventricular arrhythmias. The effective rate is 75-80%. Oral 100-150mg, 4 times a day. Common side effects are caused by Diuretic dysfunction due to anticholinergic effect, dry mouth and blurred vision. Negative muscle strength has a significant effect, so it can not be easily used with β-blockers and verapamil. Heart failure, glaucoma, urinary retention, conduction block, sick sinus syndrome, etc. should be contraindicated or used with caution, and pregnant women should not use it.


(4) Amperidine (Apridine)

This is effective for both ventricular and supraventricular arrhythmias. The toxic and therapeutic doses of this drug are very close. The dosage should be small, 25-50mg, 2 daily Times. Nervous system side effects are common, including dizziness, tremor, diplopia, epilepsy-like convulsions, etc., and can be used when other drugs are ineffective.


(5) Lidocaine

This medicine is effective for frequent ventricular premature, ventricular tachycardia, and ventricular fibrillation, including acute myocardial infarction, digitalis poisoning, and surgery, and it can increase the threshold of ventricular fibrillation, and the ventricular shock cannot be recovered Rhythms may be re-shocked with lidocaine, which may lead to cardioversion. For intravenous administration, first give a load of 50-100mg, give 50mg as appropriate for 5-10 minutes, not more than 300mg in the first hour, and maintain the amount of 1-3mg / min. The drug has small toxic and side effects. When it is used too much, it can cause drowsiness, muscle tremor, convulsions, and even sinus stagnation, and atrioventricular block. Heart failure, liver damage, and the elderly should be reduced as appropriate.


(6) Mexiletine

This is similar to lidocaine but can be taken orally. Mainly used for early ventricular and ventricular tachycardia. The oral dose is 0.1 to 0.2 g, once every 6 to 8 hours. For the first time, 100 to 200 mg can be instilled intravenously within 15 to 20 minutes, and then 200 mg can be given within 2 to 3 hours. Side effects are mild. The main side effects include neurological symptoms such as nausea, vomiting and ataxia, tremors, dizziness, and blurred vision.


(7) Tocainide

Its effects are similar to lidocaine. It is mainly used for ventricular arrhythmias. The oral dose is 0.3-0.6g, once every 8-12 hours. The side effects are mild and similar to those of slow heart rhythm.


(8) Sodium phenytoin (Diphenylbydantion)

This is currently mainly used for ectopic heart rhythm caused by digitalis response. Intravenous injection of 100-125mg, slow injection within 3-5 minutes, can be repeated every 5-10 minutes, a total of 3-4 times. Rapid intravenous administration can cause hypotension, collapse, and even death. Special attention should be paid.


(9) Ethmozine (Ethmozine)

This is a phenothiazine derivative, suitable for various premature beats, paroxysmal supraventricular tachycardia or short paroxysmal tachycardia, or slow down the ventricular rate, multipurpose Take orally, 400-800mg tincture daily, divided into 3-4 times. Intravenous administration is 1.8 mg / kg diluted in 20 ml of glucose saline and injected for 5-10 minutes. Small side effects, mainly dizziness, nausea, poor appetite, can also cause sinoatrial block. Prolonged P-R and widened QRS can disappear after stopping the drug. Atrioventricular block, sinoatrial block, sick sinus syndrome, liver and kidney dysfunction should be used with caution.


(10) Propafenone

The drug effect is similar to quinidine, but it is stronger than quinidine, and has mild anti-sympathetic and slow channel block effects. It can be used to treat recurrent supraventricular and ventricular arrhythmias. ; It can recover some atrial fibrillation and prevent its onset; It can block additional bundle reentry, and it has a better effect on preexcitation syndrome combined with atrial fibrillation or supraventricular tachycardia. It is more effective for arrhythmia related to sympathetic nerve excitation . The oral dose is 150mg, 3 to 4 times a day, the maintenance amount is 150mg, 2 to 3 times a day, and the intravenous 70mg glucose 20ml each time, the drug is generally well tolerated. The main side effects are gastrointestinal symptoms, headache, dizziness, taste disorders, etc .; adverse reactions of the cardiovascular system, which mainly cause conduction disorders, including atrioventricular or bundle branch block, sinus arrest and so on. Intravenous injection can cause a significant drop in blood pressure. This medicine has an inhibitory effect on the myocardium. Those with left ventricular dysfunction can induce and aggravate heart failure, so they have heart dysfunction, and those with hypotension and conduction block should be disabled or used with caution.


(11) Flecainide is a highly effective inhibitor of early morning drugs, which is worse for early morning. The efficacy of stopping and preventing supraventricular tachycardia and ventricular tachycardia is reliable, and the effect of controlling atrial flutter and atrial fibrillation is poor, and the prevention of seizures is effective. It can significantly prolong the effective refractory period of bypass and inhibit the reverse conduction of bypass. It is a very promising drug for the treatment of pre-excitation syndrome with tachyarrhythmia. The oral dose is 100 mg twice daily, which can be gradually increased, not exceeding 300 -400mg / day, intravenous infusion 2mg / kg. This medicine has mild negative inotropic effect and prolongs myocardial refractory period, prolongs P-R, widens QRS, and can aggravate heart failure in those with left ventricular dysfunction, occasionally causing arrhythmia, and other side effects. There are abdominal pain, bloating, headache, drowsiness, dry mouth, nausea, and vomiting.


(12) β-blockers are mainly used to block or reduce the excitatory effect of sympathetic nerves on the myocardium, and are suitable for refractory sinus tachycardia, supraventricular premature beats, tachycardia, and slowing the ventricular rate of atrial fibrillation Can be used with digoxin. Premature ventricular or ventricular tachycardia that occurs when exercise or excitement increases heart rate may also be effective. Premature ventricular or ventricular tachycardia that occurs during mitral valve prolapse may be related to sympathetic nerves and has a good effect. Commonly used is propranolol, 30-200mg daily, orally in 3 to 4 times. The main side effects are sinus bradycardia, atrioventricular block, exacerbation of heart failure, and bronchospasm. For asthma, heart failure, sick sinus syndrome, atrioventricular block, shock, etc. are disabled. Cardiac selective (ie, β1 receptor) blockers, such as aminoamidamine, have little effect on the bronchi, so it is not easy to cause bronchospasm. The oral dose is 25-50mg, 1-2 times a day.


(13) Amiodarone (Amiodarone) is a broad-spectrum antiarrhythmic drug. It is effective for supraventricular, ventricular, and pre-excitation syndrome combined with arrhythmia, but its toxicity is obvious, so it is currently proposed to be ineffective for other drugs. For patients, take 200mg orally 2-3 times a day, and gradually reduce the dose after the effect. In case of emergency, intravenous injection, 5mg / kg, 2 to 3 times, or infusion within 15-20 minutes. Common side effects are corneal hyperpigmentation, a few cases of hyperthyroidism or hypothyroidism, disappeared after discontinuation of the drug, the heart can cause sinus bradycardia or atrioventricular block, Q-T prolongation is common, if the prolongation is 25% before medication, The drug needs to be discontinued immediately. Occasionally, torsional ventricular tachycardia and ventricular fibrillation may occur, and the side effects are related to the dosage. The dosage in China is relatively small.


(14) Bretylium Tosyleate It is mainly used in critical situations such as refractory ventricular tachycardia and ventricular fibrillation, which can increase the threshold of ventricular fibrillation. When ventricular fibrillation shock is not effective, bromobenzylamine can be injected and then shocked. Reinstate it. Ventricular fibrillation without shock can be intravenously injected with brom benzylamine, 5mg / kg plus 5% glucose 40ml, 10-20 minutes, the main side effects are hypotension and nausea, vomiting, blood pressure should be closely monitored.


(15) Verapamil has an inhibitory effect on the sinoatrial node and the atrioventricular node, prolongs the effective refractory period of the atrioventricular node, and is the drug of choice for terminating atrioventricular node reentry and atrioventricular reentrant tachycardia. It can also slow the ventricular rate of atrial fibrillation and atrial flutter, but only a few can be cardioversion, can treat early atrial prevention of supraventricular recurrence, oral dose 40-120mg, 3 times a day, intravenous 5mg each time dissolved in glucose slowly Bolus. Side effects are dizziness, heart failure, pregnant women are generally not suitable for use, avoid using with beta blockers.


(16) Adenosine triphosphate (ATP): It has been reported that this medicine treats supraventricular tachycardia, which has fast effects and good effects, but has many side effects. Usually 200mg / time rapid intravenous injection. Adverse reactions include dizziness, nausea, flushing, sinus node pause, atrioventricular block, and Alzheimer’s syndrome.


(17) Berberine

In recent years, berberine has been found to have antiarrhythmic effects through pharmacological tests and clinical observations. Animal tests have shown that the drug slightly reduces the rate of phase 0 rise, prolongs the time of myocardial action potential and effective refractory period. With the exception of mild gastrointestinal symptoms, there are no other side effects. Oral administration is usually 0.3-0.4 g, 3-4 times a day.


III. The issues that should be paid attention to when using antiarrhythmic drugs

(1) First of all, you should be familiar with the pharmacological effects of various drugs, choose a treatment plan according to the arrhythmia and the electrophysiological characteristics of the drug, and perform electrophysiological acute drug tests on some refractory arrhythmias.


(2) Utilize pharmacokinetic parameters that reflect drug absorption, distribution, metabolism, and excretion to guide clinical applications.


(3) Pay attention to drug interactions to reduce adverse reactions. For example, those taking digoxin plus quinidine, verapamil, amiodarone, and arrhythmia can increase the concentration of digoxin and easily cause digitalis toxicity. The combined use of antiarrhythmic drugs can improve the efficacy and can also produce Harmful effects, such as the combination of amiodarone and IA drugs can make Q-T significantly prolonged or associated with torsional ventricular tachycardia.


(IV) Pay attention to the arrhythmogenic effect of antiarrhythmic drugs, that is, aggravate or produce arrhythmia. Almost every antiarrhythmic drug has this effect, and the estimated incidence is above 10%. It is more common in organic heart disease and left heart Patients with dysfunction, persistent ventricular tachycardia, and multiple antiarrhythmic drugs. Clinically more common patients such as IA (quinidine, procainamide, diisopropylpyridine) and class III (amiodarone and Sotalol) drugs can cause torsional VT. ICs (flucaramide, incaramide, and cardiac rhythm) can accelerate the original ventricular tachycardia, extend the duration, and even become continuous.





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