Pediatric paroxysmal ventricular tachycardia
Introduction
Introduction to paroxysmal ventricular tachycardia in children Paroxysmal ventricular tachycardia (PVT) refers to paroxysmal tachyarrhythmia occurring below the His bundle and its bifurcation. ECG features: 1QRS wave width, deformity, T wave and half wave direction Conversely; 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 and needs urgent treatment. basic knowledge The proportion of sickness: 0.01% Susceptible people: children Mode of infection: non-infectious Complications: heart failure, shock, syncope, sudden death
Cause
Pediatric paroxysmal ventricular tachycardia
Severe myocardial disease (35%):
Children with structural heart disease, more common in severe myocardial diseases, such as myocarditis, dilated cardiomyopathy, arrhythmogenic right ventricular dysplasia, hypertrophic cardiomyopathy, myocardial Purkinje cell tumor is infant ventricular tachycardia The common cause, after ventricular incision, especially in the late stage of radical surgery for elderly patients with tetralogy of Fallot, may occur ventricular tachycardia, or even sudden death, PVT occasionally seen in complete atrioventricular block, abnormal coronary origin and Kawasaki disease Patients with myocardial infarction.
Hyperkalemia (20%):
Extracardiac factors such as hyperkalemia caused by hypoxia and congenital adrenal hyperplasia can lead to ventricular tachycardia. Most of these PVTs are self-reentry agonists, and a small number of autonomic activities may be caused by late depolarization.
Drug poisoning (20%):
Drug poisoning (digitalis, expectorant, adrenaline, etc.), arrhythmogenic effects of antiarrhythmic drugs (quinidine, flecainide, amiodarone, etc.), acidosis.
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. The characteristic of autonomous arrhythmia is that it cannot be induced and terminated by sub-speed or over-speed pacing and pre-stimulation. It is often manifested as warm-up, ie in tachycardia. At the beginning of the heart rate gradually increased, we do not yet know which pediatric arrhythmia is a true self-discipline mechanism.
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, the DAD increased heart rate within a certain range when the fast, also known as tachycardia-dependent, the EAD formation mechanism more complicated.
At present, it has not been fully elucidated that 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 the following argument, namely The effect of these factors is that the background potassium current (GK1) is weakened, and some inward current (INa or ICa) is enhanced, causing the negative value of the intracellular potential to decrease, delaying the repolarization or forming the second overshot, ie EAD, which is believed to be EAD is associated with arrhythmias associated with cell damage and trauma, and thus may explain some of the ventricular arrhythmias that occur after cardiac surgery and arrhythmogenic effects during drug therapy. DAD is a threshold variation of transmembrane potential, Occurred at the end of the action potential at the 3rd phase or the 4th phase, the DAD is not caused by the direct influx of Ca2, but by the transient inward current (ITi) caused by the abnormal increase in the Ca2 concentration in the cardiomyocytes. The amplitude of the DAD depends on the perimeter of its triggering activity. When the perimeter is short enough, it can generate its own 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.
Prevention
Pediatric paroxysmal ventricular tachycardia prevention
Active prevention of congenital heart disease; active treatment of primary disease, prevention and treatment of electrolyte imbalance and acid-base imbalance, such as various gastrointestinal disorders, uremia, rheumatic fever, viral myocarditis, cardiomyopathy, Kawasaki disease, nervous system factors, hypothermia, anesthesia and Arrhythmia caused by drug poisoning and the like.
Complication
Pediatric paroxysmal ventricular tachycardia complications Complications, heart failure, shock, fainting
Often complicated by heart failure, shock, syncope and even sudden death. Suddenly, the patient suddenly felt palpitation and increased heart rate. It lasted for several minutes, hours to days, and suddenly returned to normal heart rate. At the time of the attack, the patient felt guilty, chest tightness, discomfort in the precordial area, and swelling of the head and neck, and a sense of jumping. People without heart disease generally have no significant impact, but the attack time is long. When the heart rate is more than 200 beats per minute, the patient has black eyes, dizziness, fatigue, nausea and vomiting, and even sudden fainting and shock. Patients with coronary heart disease have tachycardia and often induce angina.
Symptom
Pediatric paroxysmal ventricular tachycardia symptoms common symptoms palpitations, tachycardia, irritability, chest tightness, heart failure, shock, sudden death, syncope, cardiac arrest, dizziness
The child developed PVT on the basis of heart disease, which was a persistent episode. Infant myocardium Purkinje cell tumor often caused endless ventricular tachycardia. 20 cases of Myocardial Purkinje cell tumor were reported. The age of onset was <26 months. On average, 10 months, all showed endless VT, 15 cases of cardiac arrest or heart failure, PVT children with heart rate increased, 150 ~ 250 times / min, infants up to 300 times / min, more irritability, Heart palpitations, chest tightness, dizziness and other symptoms, severe heart failure, cardiogenic shock, syncope and even sudden death, the prognosis depends on the severity of the underlying heart disease.
Examine
Pediatric paroxysmal ventricular tachycardia
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 contraction more than 3 consecutive times, QRS wave wide deformity, baby QRS time can 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, and the ventricular rate is faster than the 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 QRS 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
Diagnosis and diagnosis of paroxysmal ventricular tachycardia in children
diagnosis
According to the medical history, clinical manifestations, and ultimately rely on electrocardiogram to confirm the diagnosis.
Differential diagnosis
Paroxysmal ventricular tachycardia should be distinguished from non-paroxysmal ventricular tachycardia, which is an accelerated ventricular autonomic rhythm with a ventricular rate similar to or slightly faster than sinus rhythm. Does not cause hemodynamic changes, children are often asymptomatic, PVT and PS-VT with wide QRS wave identification as previously described PSVT, intra-section.
(1) The speed of the room at the junction of the room junction:
1 esophageal atrial pacing can induce and terminate the attack.
The 2 compartment conduction curve was interrupted.
3 slow-fast: RPE<70ms per="" rpe="">1; fast-slow: RPE>70ms, PER/RPE<1.
The 4PV1-PE time interval is close to zero.
(2) The speed of the room bypass road reentry room:
1 esophageal atrial pacing can be induced and terminated.
The 2 compartment conduction curve is uninterrupted.
3 As the atrial pacing frequency increases, the pre-shock gradually becomes apparent.
4RPE >70ms, forward PER/RPE >1; reverse PER/RPE<1 pv1-pe="">30ms, the left side channel is negative, and the right side channel is positive.
(3) Self-disciplined atrial tachycardia:
1 esophageal atrial pacing can not be terminated and induced.
2PER/RPE<1 rpe="">70ms.
