What about tachycardia, myocardial ischemia, angina pectoris and hypotension?

Brief introduction of disease Ventricular tachycardia (VT): referred to as VT for short, refers to the heart rhythm composed of three or more consecutive premature beats originating from the ventricle, and the frequency is greater than 100 beats/min. If ventricular tachycardia is induced by the stimulation of cardiac electrophysiological examination procedure, it must last for 6 or more consecutive ventricular beats. Ventricular tachycardia is more common in patients with organic heart disease, and it may be accompanied by hemodynamic changes when the attack lasts a little longer. Therefore, the clinical situation is more urgent, which is one of the common emergencies in the cardiovascular system. There are many classification methods of ventricular tachycardia, which are generally divided into autonomic, reentrant and triggered ventricular tachycardia according to the pathogenesis. Other classification methods are [1]: according to the duration of 1. Persistent ventricular tachycardia refers to the time when ventricular tachycardia reaches or exceeds 30 seconds, or severe hemodynamic changes occur although it is less than 30 seconds. In fact, ventricular tachycardia attacks lasting 15 seconds usually last for 30 seconds or more. 2. The duration of non-persistent ventricular tachycardia is less than 30 seconds, and it can be automatically terminated within 30 seconds. According to the attack pattern of ventricular tachycardia, it is classified as 1. Unimodal ventricular tachycardia refers to a stable and single QRS waveform when ventricular tachycardia attacks, and most ventricular tachycardia are of this type. According to QRS waveform, it can be divided into right bundle branch block ventricular tachycardia and left bundle branch block ventricular tachycardia. 2. Polymorphic ventricular tachycardia means that when ventricular tachycardia occurs, its QRS waveform is different. It is generally believed that there are five or more QRS waves in succession, which are unstable in shape, have no clear equipotential lines, and are not synchronized on multiple leads recorded at the same time, which is called polymorphic ventricular tachycardia (torsade de pointes). According to whether ventricular tachycardia is complicated with organic heart disease, it can be divided into pathological ventricular tachycardia and idiopathic ventricular tachycardia. According to the different origins of ventricular tachycardia, idiopathic left ventricular septal ventricular tachycardia is also called branch ventricular tachycardia. The starting point of the left posterior branch is the most common, which can be at the distal end of the left posterior branch (near the apex) or at the proximal end of the left posterior branch (near the base), and the most common interval between the two is 1/3. Ventricular tachycardia in left ventricular outflow tract refers to ventricular tachycardia originating from left ventricular outflow tract above or below aortic valve. Ventricular tachycardia originating from the right ventricle can be divided into right ventricular outflow tract ventricular tachycardia and non-right ventricular outflow tract ventricular tachycardia. Non-right ventricular outflow tract ventricular tachycardia is generally confined to right ventricular apex, right ventricular inflow tract and right ventricular anterior wall [2]. Other classifications clinically have some special types of ventricular tachycardia. Such as ventricular tachycardia with genetic background (long QT syndrome, short QT syndrome and Brugada syndrome, etc.). ); Ventricular tachycardia with special clinical and ECG characteristics or electrophysiological mechanism (such as catecholamine sensitive ventricular tachycardia, branched ventricular tachycardia and torsade de pointes, etc.). Etiology and pathogenesis Ventricular tachycardia is common in all kinds of organic heart diseases, especially in patients with extensive and severe myocardial lesions, such as coronary heart disease with cardiac insufficiency or ventricular aneurysm after acute myocardial infarction. After myocardial infarction, abnormal ECG activity, abnormal wall motion, abnormal bundle branch conduction and heart failure provide pathophysiological basis for the occurrence of ventricular tachycardia. Epidemiological data show that more than 90% of dilated cardiomyopathy has persistent ventricular tachycardia. Autopsy found that13 patients with ventricular tachycardia had extensive endocardial scar formation, and more than 50% patients' myocardial tissue was replaced by fibrous tissue, which provided anatomical basis for reentry formation. Arrhythmogenic right ventricular dysplasia, hypertrophic cardiomyopathy and severe myocarditis are all due to the disorder of myocardial cell arrangement, myocardial ischemia and decreased myocardial function, which form the pathological basis of ventricular tachycardia. A few patients have no clear evidence of organic heart disease, such as primary QT interval prolongation syndrome and mitral valve prolapse. Ventricular tachycardia disappeared after the cause was corrected, such as digitalis poisoning, sympathomimetic overdose, secondary QT interval prolongation caused by antiarrhythmic drugs and tricyclic antidepressants, QT interval prolongation caused by antimony and chloroquine, hypokalemia or hypomagnesemia. In addition, hypothermia anesthesia, cardiopulmonary surgery or mechanical stimulation of cardiac catheter can also lead to various tachycardia. The electrophysiological mechanism of ventricular tachycardia is mostly reentry, and its reentry ring is mostly located in the ventricle, and bundle branch reentry is rare. A few of them are autonomic nervous abnormalities or secondary excitement after graduation, and this kind of ventricular tachycardia can't usually be terminated by electrophysiological program stimulation. The inducement of clinical manifestations of ventricular tachycardia is often myocardial ischemia or cardiac insufficiency, or there may be no obvious inducement. During the attack of ventricular tachycardia, the degree of hemodynamic dysfunction is more serious, and the performance of insufficient blood supply to heart and brain organs is often obvious. The clinical symptoms of symptomatic ventricular tachycardia pay little attention to the ventricular rate, duration, basic heart disease and cardiac function at the time of attack. Patients with non-persistent ventricular tachycardia are usually asymptomatic. Persistent ventricular tachycardia is often accompanied by obvious hemodynamic disorder and myocardial ischemia symptoms. Clinical symptoms include palpitation, hypotension, syncope, shortness of breath and angina pectoris [3]. Signs auscultation heart rhythm is slightly irregular, the first and second heart sounds are split, and systolic blood pressure can change with the heartbeat. If complete atrioventricular separation occurs, the intensity of the first heart sound often changes, and huge A waves appear intermittently in the jugular vein. When the ventricular pulse propagates reversely and continues to capture the atrium, the atrium and ventricle contract almost simultaneously, and the jugular vein presents a regular and huge A wave. Auxiliary examination of electrocardiogram 1. QRS wave is ventricular waveform, widened and deformed, QRS time limit >; 0.12s, a few ventricular tachycardia originating from his bundle bifurcation cannot exceed 0.12s. 2. There are often secondary ST-T changes. 3. Ventricular frequency 140-200 beats/min, regular or slightly irregular, with occasional RR interval of 0.33 seconds. 4. Sinus rhythm can continue to exist alone, forming atrioventricular separation. 5. Occasionally sinus P wave conducts and captures the ventricle, forming early narrow QRS (ventricular capture), which is the same as or slightly different from QRS wave in sinus rhythm (combined with frequency-dependent indoor differential conduction); Sometimes sinus P wave captures part of the ventricle and forms ventricular fusion wave with ventricular ectopic beat, which has the characteristics of sinus and ventricular QRS. Ventricular capture and fusion wave are powerful evidence for the diagnosis of ventricular tachycardia. 6. When ventricular tachycardia occurs, most QRS waves have the same shape, or they can have multiple shapes, which are called simple and polymorphic ventricular tachycardia respectively. 7. Ventricular tachycardia is often induced by premature beats, and its shape is usually consistent with premature beats, but also inconsistent. 8. Ventricular tachycardia can be terminated automatically, and the frequency and rhythm often change before termination; It can also be transformed into ventricular flutter and ventricular fibrillation, and the ventricular rate is accelerated before transformation. 9. ECG characteristics of special type of ventricular tachycardia: 1) Idiopathic ventricular tachycardia with right ventricular outflow tract, in which V 1 lead and V2 are rS type, and the transition zone is in V3 or V4 lead, and the time limit is >; 0. 12 second. 2) The origin of left posterior branch ventricular tachycardia is close to the basal part, and QRS complex wave is the type of right bundle branch block+left anterior branch block, with the time limit of 0.1~ 0.14 seconds. Left or right deviation of the electrical axis can lead to ventricular atrial separation or a certain proportion of conduction. Dynamic electrocardiogram is helpful to diagnose and evaluate ventricular tachycardia, especially for patients with repeated syncope. Electrophysiological examination Intracardiac electrophysiological examination can make a definite diagnosis, explain the mechanism of ventricular tachycardia, terminate tachycardia, determine the origin of tachycardia and guide catheter ablation treatment. Intracardiac electrophysiological examination is of great significance in judging the severity of ventricular tachycardia and predicting the risk of sudden death. The treatment of paroxysmal ventricular tachycardia is critical, which can easily lead to ventricular arrest or ventricular fibrillation and death, so it must be dealt with against time. If it is caused by drugs, stop using such drugs immediately. Disease treatment includes direct current cardioversion, drug therapy, surgical treatment, interventional therapy and other treatment methods [4]. DC cardioversion During the attack of ventricular tachycardia, DC cardioversion can immediately stop ventricular tachycardia in most cases. When ventricular tachycardia is accompanied by acute hemodynamic disorders such as hypotension, shock, acute heart failure or severe angina pectoris, it should be the first choice. The energy should be 150~200J at first. When the effect is not good, the energy should be increased in time, and sometimes 300~360J can be directly selected for a rainy day. Drug therapy is 1. Lidocaine 100mg intravenous injection. If it is ineffective, inject 1 time at the rate of 0.5mg/kg per minute, the total amount shall not exceed 300mg within 30 minutes, and the effective maintenance amount shall be 1 ~ 4 mg/min. 2. intravenous injection of procainamide 50~ 100ng, repeated every 5 minutes/time, the total amount can reach 1 g within 1 hour, and the maintenance dose is 2 ~ 5 mg/min; 3. Brombenzylamine 5mg/kg 10 min, and then1~ 2 mg/min; 4. intravenous amiodarone150mg; 5. Propafenone 70mg intravenous injection; 6. If the electrocardiogram shows that ventricular tachycardia is R-on-ST segment ventricular premature beats, verapamil 5 ~10 mg can be injected intravenously first; 7. Ventricular tachycardia caused by digitalis poisoning can be treated with phenytoin sodium and potassium salt; 8. If there is no obvious reason for young people, it is often through the induction of activity or emotional excitement to obtain obvious curative effect. However, some antiarrhythmic drugs are not effective or even harmful in preventing the recurrence of ventricular tachycardia and reducing sudden cardiac death, especially for patients with organic heart disease complicated with ventricular tachycardia. 9. Torsion de pointes ventricular tachycardia secondary to long QT syndrome can be stopped and prevented from recurring in a short time by increasing basal heart rate and intravenous magnesium sulfate at the same time of etiological treatment. Congenital long QT syndrome complicated with torsade de pointes can be treated with beta blockers. Interventional therapy 1. Transcatheter radiofrequency ablation: Transcatheter radiofrequency ablation can successfully treat ventricular tachycardia, which is an ideal treatment method at present. Ablation therapy has a very good effect on ventricular tachycardia without organic heart disease, such as idiopathic left ventricular tachycardia or right ventricular tachycardia, and the success rate is above 90 ~ 95%. ① High atrial electrode-femoral vein; ② His bundle electrode-femoral vein; ③ Right ventricular apical electrode-femoral vein; ④ Coronary sinus electrode-cephalic vein or left subclavian vein; Large head ablation electrode-femoral arteriovenous; Auricular electrode-femoral vein 2. Implantable cardioverter defibrillator (ICD) treatment: ICD is a device that can automatically identify ventricular tachycardia and ventricular fibrillation after implantation in the body, and terminate ventricular tachycardia and ventricular fibrillation through electric defibrillation. It has good curative effect on persistent ventricular tachycardia, especially ventricular arrhythmia with high risk of sudden death, and can improve the prognosis of patients, especially for patients with organic heart disease complicated with obvious cardiac insufficiency. Surgical treatment The indication of surgical treatment is ventricular aneurysm formed after myocardial infarction or the focus of arrhythmogenic right ventricular hypoplasia cardiomyopathy, and it is feasible to remove the related diseases of ventricular tachycardia. It is feasible to map the endocardium or epicardium of the heart without organic lesions and cut the corresponding lesions. It is reported that cervicothoracic sympathectomy is effective for long QT syndrome. It has also been reported that resection of hypertrophic ventricular septum in hypertrophic cardiomyopathy can prevent sudden death. Prognosis of the disease Ventricular tachycardia has a serious prognosis, which is easy to develop into ventricular fibrillation and has a high mortality rate. It should be treated immediately. Most ventricular tachycardia can be corrected if it can be diagnosed early and treated in time. Typical polymorphic ventricular tachycardia is more common in coronary heart disease, and ventricular tachycardia may or may not be accompanied by acute myocardial infarction. Polymorphic ventricular tachycardia is accompanied by a very short rhythm interval, and its clinical manifestations are palpitation, dizziness and syncope, and repeated attacks can lead to death. Because idiopathic ventricular tachycardia has no definite heart disease and strong tolerance to tachycardia, long-term clinical follow-up shows that there are few reports of arrhythmia death (sudden death) so far, so the prognosis is good. Adrenaline-dependent torsade de pointes is QTc interval >: 0.60 seconds. Tachycardia, sudden death history and ineffective treatment with propranolol are high-risk indicators of LQTS. The prognosis of patients is poor, and the annual mortality rate is 9%. The mortality rate of patients with symptomatic torsade de pointes after the first syncope attack 1 year is over 20%, and the mortality rate in1year is as high as 50%. The first step to prevent disease and recurrence is to remove the causes, such as treating myocardial ischemia, correcting water-electrolyte imbalance, treating hypotension and hypokalemia, and treating congestive heart failure, which is helpful to reduce the number of ventricular tachycardia attacks. When sinus bradycardia or atrioventricular block occurs, the ventricular rate is too slow, which is beneficial to the occurrence of ventricular arrhythmia. Atropine or artificial cardiac pacing can be used to increase the heart rate. Considering the toxic and side effects of long-term drug therapy, patients with negative ventricular late potential, non-persistent or programmed stimulation can not induce persistent ventricular tachycardia do not necessarily need antiarrhythmic drugs. For example, patients with positive ventricular late potential, persistent recurrent attacks or programmed stimulation can induce ventricular tachycardia, which is quite dangerous, so antiarrhythmic drugs are needed to prevent recurrent ventricular tachycardia. Reference 1. Chen Haozhu, Lin Guowei and so on. Practical internal medicine. People's Health Publishing House, 14062. Ma Changsheng, Zhao Xue and so on. Cardiac electrophysiology and radiofrequency ablation, Liaoning Science and Technology Press, 170-2033. Lu Zaiying, Zhong Nanshan. Internal Medicine 7th Edition, People's Health Publishing House, 2224. Wang et al., second edition of eight-year internal medicine, People's Medical Publishing House, pages 235-237.