Ventricular tachycardia in children

Introduction to pediatric ventricular tachycardia Ventricular tachycardia (VT), referred to as ventricular tachycardia, refers to a rapid arrhythmia occurring below the His bundle and its bifurcation. ECG features: 1QRS wave width, deformity, T wave is mostly opposite to the main wave 2 compartment separation; 3 ventricular capture or ventricular fusion wave; 4 ventricular tachycardia. Reported about 6% of rapid arrhythmia, is a serious tachyarrhythmia, can develop into ventricular fibrillation, causing sudden cardiac death, hemodynamic changes due to ventricular tachycardia, often causing palpitation, chest tightness, difficulty breathing, Symptoms such as blackness, syncope and shock, therefore, ventricular tachycardia is a pediatric emergency requiring urgent treatment. Pediatric VT includes a group of different natures from the etiology, pathogenesis, clinical manifestations, ECG characteristics, prognosis and treatment response. Sexual tachycardia refers to three or more consecutive pulsations originating from the ventricle. The ventricular rate of ventricular tachycardia in children is >120 beats/min (>100 beats/min for adults). The current opinion on the minimum heart rate limit for infants and young children is not uniform. It is recommended that the heart rate for ventricular tachycardia in a specific population should be higher than 25% of the normal sinus heart rate. basic knowledge The proportion of the disease: 0.05% of the specific population Susceptible people: children Mode of infection: non-infectious Complications: chronic cardiac insufficiency pulmonary edema cardiogenic shock

Causes of ventricular tachycardia in children

(1) Causes of the disease

Cause

There are many causes of ventricular tachycardia in children, which can be seen in the cardiovascular system itself, and also in heart damage caused by various other diseases, such as drugs, poisoning, electrolyte imbalance, etc., and some unexplained "normal" people".

(1) Physiology: In infants and children, some patients with ventricular tachycardia have no structural heart disease and other systemic diseases, and they often attack during exercise.

(2) Heart disease: Children often have viral myocarditis, congenital heart disease and heart disease during and after surgery, cardiomyopathy, rheumatic heart disease, cardiac tumors, etc.

(3) Drug and toxic effects: such as digitalis, arrhythmia effects of various antiarrhythmic drugs, other drug poisoning or allergies can cause ventricular tachycardia.

(4) electrolyte imbalance and acid-base imbalance: hypokalemia caused by various causes, hypocalcemia, hypomagnesemia is a common cause of ventricular tachycardia.

(5) systemic diseases: severe hypoxic asphyxia, SLE, severe infection can cause ventricular tachycardia after myocardial injury.

2. Classification

The electrocardiographic manifestations of ventricular tachycardia, duration of onset and clinical characteristics are different. There is no unified classification method. This paper combines domestic and foreign reports to classify according to ECG manifestations, seizure patterns and clinical changes.

(1) Classification according to ECG performance:

1 monoventricular tachycardia (monoventricular tachycardia): refers to the ventricular tachycardia episodes, the same on the same lead of the electrocardiogram QRS group form only a single, but according to different causes, the origin of tachycardia is different, There are some differences in the morphology of QRS complexes. Monomorphic ventricular tachycardia can be short-term or persistent.

2 bidirectional ventricular tachycardia: also known as "bidirectional tachycardia" or "bidirectional ventricular rhythm", refers to the heartbeat of the two QRS-T waveforms alternately formed on the same ECG lead Overspeed, bidirectional ventricular tachycardia appears as a rapid two QRS-T waveforms alternately appearing in the following form: A. QRS wave time <0.10s, B. left front branch and left posterior branch block pattern alternately appear , C.QRS time is >0.10s, wide deformity, D. One QRS wave time <0.10s, the other >0.10s.

The mechanism of bidirectional ventricular tachycardia has not been fully elucidated. There are several explanations: A. Dual-source ventricular tachycardia, alternating ectopic beats in the ventricle, B. A QRS wave from the room Rhythm point, another QRS wave from the ventricle, C. supraventricular tachycardia with alternating left anterior branch and left posterior branch block, which is a common principle of bidirectional ventricular tachycardia confirmed in recent years, D Single-source ventricular tachycardia with alternating reentry indoor differential conduction, this type is rare in clinical, mainly seen in severe organic heart disease or digitalis poisoning and hypokalemia patients, for ventricular fibrillation Precursor, the prognosis is serious.

3 Parasitic ventricular tachycardia (also known as ventricular tachycardia), also known as ventricular parallel tachycardia, is based on ventricular parallel rhythm, ventricular parallel heart rhythm refers to ventricular subendocardial Purkinje fiber The ectopic rhythm of the network has a protective afferent block around it. The sinus agitation can not be invaded, so that the ectopic pacemaker can automatically depolarize according to its own frequency and compete to control the ventricle, while the ectopic rhythm is also around. There is often an efferent block, and the excitement cannot be transmitted to the surrounding area every time. Only when there is no efferent block or the refractory period of the surrounding myocardium can cause an ectopic agitation, when the ectopic pacemaker is efferent. When the block disappears, the parallel ventricular tachycardia is formed, and the electrocardiogram characteristics of the parallel ventricular tachycardia are:

A. There is an independent ventricular ectopic rhythm.

B. In each group of short-term ventricular ectopic rhythms, the first interventricular ectopic interval is not fixed.

C. The distance between each ventricular ectopic beat is a multiple of the RR period of ventricular tachycardia, or the minimum common divisor can be measured between RRs.

D. The frequency is close to the sinus heart rate, which is 100-140 times/min, and occasionally 140-220 times/min.

E. Visible ventricular fusion waves.

4 polymorphic ventricular tachycardia (polymorphic ventricular tachycardia): refers to the occurrence of tachycardia, the presence of more than three forms of QRS complex in the same lead of the electrocardiogram, according to the pleomorphic ventricular tachycardia There are two categories without the extension of the QT interval.

A. Polymorphic ventricular tachycardia is associated with prolongation of QT interval. Because most of these types are torsades ventricular tachycardia, this type is called QT extension and ventricular tachycardia or torsades de pointive ventricular according to Jackman's recommendation. The tachycardia is characterized by an increase in the QT before and after the onset of the attack. When the tachycardia occurs, the QRS complex is irregularly twisted up and down along a baseline with a frequency of >200 beats/min.

B. Polymorphic ventricular tachycardia: The QRS complex is polymorphic at the time of onset, and the QT, T or U wave is normal at baseline.

(2) According to the duration of tachycardia classification: according to the duration of ventricular tachycardia episodes, it is divided into three categories:

1 sustained ventricular tachycardia (sustained ventricular tachycardia): refers to the onset of tachycardia for more than 30s, due to long duration, can appear palpitations, chest tightness and other symptoms, severe cases may appear syncope, shock and other changes.

2 nonsustained ventricular tachycardia (nonsustained ventricular tachycardia): refers to ventricular tachycardia episodes of short duration, duration of less than 30s, due to short duration, patients often have palpitations, chest tightness and other symptoms, rare syncope, shock, etc. symptom.

3 reciprocating ventricular tachycardia (reciprocating ventricular tachycardia): continuous reentry with ventricular tachycardia, the electrocardiogram features:

A. The frequency of tachycardia is 60-250 times/min.

B. Taking QRS-P'-QRS-P' QRS-P'-QRS-P'... as the basic performance, the first heart beat is ventricular repetitive heartbeat, the QRS complex is broad and deformed, and all are P' - Normal QRS complexes.

(3) Classification according to clinical characteristics: According to the clinical characteristics of various types of ventricular arrhythmia in children, the classification of whether there is primary heart disease and treatment prognosis is:

One-stage pre-systolic ventricular tachycardia (extrasystolic ventricular tachycardia).

2 idiopathic ventricular tachycardia (idiopathic ventricular tachycardia).

3 tip torsade ventricular tachycardia (torsades de pointes).

4 catecholamine related ventricular (tachycardia).

5 arrhythmogenic right ventricular dysplasia (arrhythmogenic right ventricular dysplasia).

6 accelerated ventricular rhythm (accelerated ventricular rhythm).

(two) pathogenesis

As with adults, the electrophysiological mechanism of ventricular arrhythmias is the same as all other arrhythmias, ie, autonomic abnormalities, triggering agitation and reentry mechanisms, and it is impossible to determine the pathogenesis of a ventricular arrhythmia with current knowledge. Nor can it be inferred from the electrocardiogram. However, recognizing these possible mechanisms helps us understand the etiology, diagnosis and treatment of ventricular tachycardia.

1. Self-disciplined abnormality

Some cells with normal self-discipline, such as sinoatrial node and atrioventricular node cells, can spontaneously depolarize, trigger an action potential after the membrane potential reaches a threshold, spontaneous depolarization and maintenance of transmembrane potential of cardiomyocytes are controlled by cells inside and outside. The transmembrane flow of ions enables most cardiomyocytes to be self-disciplined under normal conditions, but self-discipline can be obtained when damaged or diseased. The abnormal self-discipline of this cell and the normal self-regulation of cardiac pacemaker cells Differently, its membrane potential has changed.

Autophagic arrhythmia is characterized by its inability to be induced and terminated by sub-speed or over-speed pacing and pre-stimulation. It is often manifested as a warm-up, that is, the heart rate gradually increases during the early tachycardia. Understanding which pediatric arrhythmias are truly self-disciplined mechanisms.

2. Trigger activation (trigger self-discipline)

Triggered activity is caused by the reaction of the post-polarization cell to the previous action potential. This post-potential occurs in the third phase of the action potential and is divided into early post-depolarization and post-delay depolarization. In 1975, the concept of triggering excitatory was first proposed. Triggering excitatory refers to the membrane oscillating post potential triggered by the heart depolarization. Because it always occurs after a depolarization, it is also called post depolarization. When the depolarization potential reaches the threshold. At the potential, a triggering action potential is generated, and because of the post-potential itself, the sequential tachycardia forms a tachycardia. It can be seen that the triggering agonism includes the after potential of the cardiomyocytes and the induced trigger arrhythmia. The post-depolarization occurs under the threshold of the previous action potential repolarization or after the repolarization is completed, which is called early after depolarization (EAD) and delayed after depolarization (delayed after depolarization, respectively). DAD), EAD occurs before the end of repolarization, that is, the third phase of the action potential, because the EAD increases when the heart rate is slow, also known as bradycardia-dependent type, DAD occurs when the repolarization is about to end or After the beam, when the DAD increases faster heart rate in a certain range, also known as tachycardia dependent.

The mechanism of EAD formation is complicated, and it has not been fully elucidated. EAD is a small potential shift generated in tissue perfusion, which occurs in the third phase of the action potential and may be related to the amplitude of the previous action potential. According to the research results, most scholars support it. The following arguments are the effect of certain factors that weaken the background potassium current (GK1) and increase some inward current (INa or ICa), causing a decrease in the intracellular potential, delaying the repolarization or forming a second overshoot. EAD, which is thought to be associated with arrhythmias associated with cell damage and trauma, can explain some of the ventricular arrhythmias that occur after cardiac surgery and the arrhythmogenic effects of drug therapy.

DAD is a threshold variation of transmembrane potential, which occurs at the end of the action potential at the 3rd or 4th phase. DAD is not formed by direct Ca2 influx, but is transient inward caused by abnormally increased Ca2 concentration in cardiomyocytes. Due to the transient inward current (ITi), the amplitude of the DAD depends on the perimeter of its triggering activity. When the perimeter is short enough, it can generate its own maintained action potential. It is because of the dependence of DAD on the driving frequency. The "triggered" rather than the self-regulatory form is also associated with reentry. In the laboratory, digoxin poisoning, hypokalemia, and catecholamines can induce DAD in myocardial tissue, but the clinical arrhythmia has not been confirmed.

3. Reentry

Reentry is the most common mechanism of rapid arrhythmia in clinical practice. The three prerequisites for forming a reentry are:

(1) There are at least two potential channels anatomically or functionally connected to the proximal and distal ends to form a conduction loop.

(2) One of the above channels has a one-way block.

(3) The unblocked channel conducts slowly, allowing the blocked channel to have enough time to restore stress. When the conduction delay and refractory period of the two channels are appropriate, a continuous forward electrical impulse is generated. Leading to tachycardia, reentry tachycardia can be induced and terminated by pre-stimulation or rapid pacing, which maintains a matching of the electrophysiological conditions of the reentry loop, which can explain some of the late ventricular rhythms after cardiac surgery Abnormal.

Pediatric tachycardia prevention

Actively prevent congenital heart disease, actively treat primary disease, prevent electrolyte imbalance and acid-base imbalance, such as various gastrointestinal diseases, uremia, rheumatic fever, Kawasaki disease, nervous system factors, hypothermia, anesthesia and drug poisoning, etc. Abnormal. Take a proper rest and avoid strenuous exercise. But when the condition is stable, pay attention to proper exercise. Increase disease resistance, avoid cold, pay attention to regular review.

Pediatric ventricular tachycardia complications Complications chronic heart failure pulmonary edema cardiogenic shock

Can be complicated by cardiac insufficiency, pulmonary edema, cardiogenic shock, ventricular fibrillation, A-S syndrome, heart enlargement, convulsions and so on. Cardiogenic shock is a syndrome in which cardiac output is significantly reduced and severe acute peripheral loop failure is caused by a severe decline in cardiac function. The cause is acute myocardial infarction, severe myocarditis, cardiomyopathy, tamponade, severe arrhythmia or chronic heart failure end-stage can cause this disease.

Pediatric ventricular tachycardia symptoms common symptoms palpitations systolic murmur arrhythmia chest tightness electrocardiogram abnormal palpebral tachycardia weakness ventricular fibrillation pale

1. Pre-systolic ventricular tachycardia is a malignant arrhythmia, which is easy to cause hemodynamic changes. Early patients have poor spirits, pale, complaining of chest tightness, palpitations, shortness of breath, rapid heart rate, heart rate, low heart sound Blunt, if not corrected in time, can develop into cardiac insufficiency, pulmonary edema, shock, etc., or ventricular fibrillation, A-S syndrome, etc., most of the pre-existing symptoms of myocardial involvement.

2. Idiopathic ventricular tachycardia can occur in children and adolescents of all age groups. It is reported that the minimum age is 1 year old, upper respiratory tract infection, exercise or mental stress and depression are often induced factors, and there is no obvious incentive. Occurrence, seizures can be manifested as sudden onset, mild palpitations, pre-cardiac discomfort and other symptoms, without syncope, shock, etc.; can also be characterized as persistent seizures, depending on the length of time may appear palpitations, chest tightness, Dizziness, even syncope, shock and heart failure, but overall tolerability, idiopathic ventricular tachycardia patients without organic heart disease, the cause of the disease is unknown, Janet et al on 18 cases Myocardial biopsy was performed in patients with ventricular tachycardia. Among them, 16 cases had abnormal myocardial tissue, so the disease was proposed as subclinical cardiomyopathy.

3. Accelerated ventricular rhythm can occur in all ages. Van Hare reports that 12 cases of neonatal accelerated ventricular rhythm, Gaum reported 4 cases of school-age children, no gender differences, because their ventricular heart rate is close to sinus Generally, no obvious hemodynamic changes occur. If accompanied by cardiac or systemic diseases, clinical manifestations mainly accompany the disease. Accelerated ventricular rhythm can be seen in normal children, often found in physical examination or routine electrocardiogram examination. Without episodes of dizziness, syncope, palpitations, and shortness of breath.

4. Torsades ventricular tachycardia can occur in children at different times, the most common symptoms are repeated syncope and (or) convulsions, often induced in exercise, stress, emotional stress, etc., infants are induced by crying and so on, The frequency of seizures was different, and some frequent episodes occurred for several days. A case was diagnosed in the Affiliated Hospital of Guangdong Medical College. It occurred once every 5 to 20 minutes, repeated for 2 days, some episodes were sparse, and a few months or even a few episodes occurred. The duration varies from a few seconds to a few minutes. The child with intermittent seizures is conscious and has no obvious symptoms. However, the author may be apathetic after 1 day. When the attack occurs, the face may appear pale or blemishes, and then there may be limb twitching or weakness. Heart rate 200 ~ 300 times / min, the heart rhythm is absolutely not complete, the heart sounds are not strong, can not even hear clearly, the intermittent auscultation is often sinus bradycardia, heart sounds weak or normal, some children suddenly die, the general situation Next, cardiac X-ray, two-dimensional ultrasound and ventricular angiography can be normal, repeated authors can appear heart enlargement and cardiac insufficiency.

5. Arrhythmogenic right ventricular dysplasia (ARVD) The incidence of ARVD is more common than that of college-age children and adolescents. Infants and young children have also reported that there are more males than females, and the clinical manifestations vary greatly. Repeated syncope, especially in severe exercise, or even sudden death, can be complicated by heart failure, mainly due to right heart failure, physical examination of jugular vein filling, normal carotid pulsation, partial heart slowly increase can occur in the anterior region of the heart, ventricular Enlargement, irregular heart rhythm, audible third, fourth heart sound, low heart sound, 3 to 4 intercostal space on the left sternal border and 1/6 to 3/6 systolic murmur in the apical area, no diastolic murmur, part The patient only had recurrent syncope and arrhythmia, no symptoms and signs of heart failure. Asymptomatic patients may have abnormal cardiac auscultation and abnormal electrocardiogram during routine physical examination. The diagnosis of ventricular tachycardia can usually be made by analyzing the surface electrocardiogram. Lead electrocardiogram recording or 12-lead 24h ECG monitoring is very helpful, because one or two monitoring leads of 24h ECG monitoring will miss some diagnostic features of ventricular tachycardia, and the apparent ECG of ventricular tachycardia For abnormal QRS waves and room separation, the QRS wave at ventricular tachycardia can be very narrow (for example, the neonatal period is as short as 60ms), and the QRS complex is also widely deformed. The QRS morphology is generally not diagnostic, and the most diagnostic sign is Separation of the chamber, the separation of the chamber usually shows that the P wave frequency is slower than the QRS wave frequency and is not associated with the QRS complex. In most cases, there is room separation during ventricular tachycardia, even in children, but sometimes it is difficult to identify. The indirect sign of chamber separation is the atrial capture of the fusion wave. The capture pattern is caused by an early normal QRS complex and subsequent ventricular tachycardia QRS fusion. The formation is due to the refractory period of the atrioventricular node and the P wave. Excited happens to reach the atrioventricular node and pass to the ventricle, which is the atrium of the ventricle. The QRS form of the fusion wave is between normal and ventricular tachycardia. Some ventricular tachycardia have stable 1:1 reverse conduction without room separation and The characteristics of atrial capture, intravenous adenosine produces a ventricular block, which can be used to confirm the diagnosis of ventricular tachycardia. If no compartment separation is found, it can be identified by echocardiography. M echocardiography shows mitral valve opening. Very irregular, regardless of the regularity of the surface electrocardiogram QRS wave, the mitral valve can not be fully open during some diastolic periods, according to this phenomenon can be diagnosed with ventricular tachycardia with room separation.

Pediatric ventricular tachycardia examination

Should be done myocardial enzyme assay, blood pH, erythrocyte sedimentation rate, anti-"O", immune function, etc., in order to determine the cause, ECG should be routinely performed, chest X-ray, echocardiography (UCG) and dynamic electrocardiogram detection, sinus rhythm The ECG helps to understand whether there is a prolonged QT interval and rare coronary abnormalities. UCG can detect mitral valve prolapse, hypertrophic cardiomyopathy, dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy and cardiac tumors. Holter monitoring can be used to understand the frequency of ventricular tachycardia, duration of onset and ventricular tachycardia. Some children need selective exercise tests, blood tests and electrophysiological examinations to determine the cause.

Electrocardiogram

There are the following common changes:

(1) ventricular premature contraction: ventricular premature beats for more than 3 consecutive times, QRS wave wide deformity, baby QRS time may not exceed 0.08s, ventricular rate 150 ~ 250 times / min;

(2) visible sinus P wave: P wave and QRS wave are independent, showing separation of the atrioventricular rate, ventricular rate is faster than atrial rate;

(3) ventricular fusion and ventricular capture may occur: pediatric VT is now divided into paroxysmal ventricular tachycardia, idiopathic ventricular tachycardia and idiopathic long QT syndrome complicated by torsade ventricular tachycardia The tachycardia is described separately.

2. Electrophysiological examination

Electrophysiological examination is not a mandatory item for patients with ventricular tachycardia. Before performing this examination, the purpose of the examination must be clearly defined and the end point of the examination must be determined. The purpose of the examination is to induce arrhythmia in clinical manifestations, and to induce a non-sustainable, non-clinical manifestation. Speed usually has no meaning. The specificity of children with ventricular tachycardia is described below.

(1) indications for electrophysiological examination of ventricular tachycardia:

1 Clear diagnosis of ventricular tachycardia, differential diagnosis of wide ORS wave tachycardia with unknown mechanism.

2 to elucidate the mechanism of ventricular tachycardia, according to its electrophysiological characteristics to identify the electrophysiological mechanism of tachycardia is reentry, self-discipline or trigger activity.

3 Determine the origin of ventricular tachycardia and guide the radiofrequency catheter ablation.

4 evaluate the feasibility of implanting an in vivo defibrillator (ICD).

5 drug electrophysiological studies, screening anti-arrhythmia drugs, evaluation of treatment effects.

6 for unexplained syncope, electrophysiological examination to see if there is arrhythmia leading to syncope, especially the clinical cause of ventricular tachycardia, such as congenital heart disease.

(2) Stimulation plan:

1 induced ventricular tachycardia: starting from a single pre-stimulation of S2, the basal circumference depends on the sinus cycle, if tachycardia can not be induced, increase the pre-stimulation to S3 or until S4, if not induced then change the basal circumference to repeat the above Pre-stimulation, the right ventricular apex is routinely selected in the stimulation site. If the stimulating site can not be induced to the right ventricular outflow tract, if the ventricular tachycardia is still not induced, intravenous infusion of isoproterenol 0.1 g / (kg · min), repeated The above steps.

2 If the ventricular tachycardia is induced, immediately evaluate its impact on hemodynamics, such as the occurrence of hemodynamic disorders to immediately terminate the ventricular tachycardia; in the case of hemodynamic stability, record the 12-lead ECG ventricular tachycardia, The ventricular tachycardia lasted for more than 30s, which was defined as continuous ventricular tachycardia. In most cases, there was room separation. There was no His bundle potential in front of V wave to facilitate the diagnosis of ventricular tachycardia. Pay attention to the atrioventricular nodal reentry tachycardia. Roomimetric reentry (Mahaim fiber) or other abnormally transmitted supraventricular rapid phase identification, if necessary, fine mapping can be found in the earliest activation site of ventricular tachycardia.

3 termination of room rate:

A. Since the speed of ventricular tachycardia is 10 to 20 times/min, the speed of pacing starts gradually, and the frequency is gradually increased.

B. Single (S2) or two (S2S3) ventricular premature stimulation termination.

C. If the above two methods are invalid, short bursts of rapid stimulation or direct current conversion can be performed.

4 understand the drug effect routine without electrophysiological examination, unless the drug treatment fails, can be used as an indication of electrophysiological examination, the purpose of the test is to know whether the drug can terminate tachycardia and / or can induce tachycardia after medication.

5 combined with electrophysiological examination for other invasive examinations, such as hemodynamic assessment and right ventricular angiography, if necessary, should be performed esophageal ECG, 24h dynamic electrocardiogram, cardiac catheterization, MRI examination.

Diagnosis and diagnosis of ventricular tachycardia in children

diagnosis

The width and narrowness of the QRS waveform are not helpful for the diagnosis. The apparently irregular wide QRS tachycardia is seen in polymorphic ventricular tachycardia (referred to as polymorphic ventricular tachycardia) or pre-excitation syndrome with atrial fibrillation ( Attenuation of narrow QRS wave tachycardia can also be seen in ventricular tachycardia or supraventricular tachycardia. The diagnosis should be made with reference to other characteristics of the above ventricular tachycardia.

In addition to the diagnosis of ventricular tachycardia by tachycardia, the electrocardiogram should be carefully examined for sinus rhythm to detect abnormalities, especially with or without QRS morphology, QT interval and U wave anomalies or pre-shock.

Differential diagnosis

Many ventricular tachycardia patients have no obvious symptoms and supraventricular tachycardia can also cause syncope; ventricular rate in children with ventricular tachycardia is 120-300 beats / min, the heart rate of supraventricular tachycardia can also be in a similar range, therefore, to have No symptoms and heart rate are difficult to distinguish ventricular tachycardia from other arrhythmias of abnormal QRS waveforms.

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