Ventricular tachycardia in the elderly

Introduction to ventricular tachycardia in the elderly Ventricular tachycardia (VT) is a rapid arrhythmia of bundle branches, myocardial conduction fibers, and ventricular muscles that occur below the His bundle bifurcation. Wellens defines it as: frequency over 100 beats/min, continuous 3 or more spontaneous ventricular depolarization activities, including monomorphic non-sustained and persistent ventricular tachycardia and polymorphic ventricular tachycardia, if cardiac electrophysiological procedures are used for cardiac electrical stimulation The induced ventricular tachycardia must be 6 or more rapid ventricular beats (frequency > 100 beats / min). Ventricular tachycardia can originate in the left ventricle and right ventricle. The frequency of persistent episodes often exceeds 100 beats/min, and the hemodynamic state may worsen. It may become atrial flutter and ventricular fibrillation, leading to cardiac origin. Sudden death requires active treatment. basic knowledge The proportion of illness: 0.001% Susceptible people: the elderly Mode of infection: non-infectious Complications: syncope, sudden death

The cause of ventricular tachycardia in the elderly

Primary cardiomyopathy (20%):

Ventricular tachycardia can occur in dilated cardiomyopathy, hypertrophic cardiomyopathy, and restrictive cardiomyopathy. Cardiac necrosis, fibrosis, lesions, myocardial loss of normal structure and morphology in patients with primary cardiomyopathy, and conduction An obstacle occurs to form a reentry, causing an episode of ventricular tachycardia. The ventricular tachycardia is a multi-bundle regurgitation ventricular tachycardia. The pacemaker is often in the left ventricle. The activation is reversed from the left bundle branch to the His bundle, and the right bundle is involved. After reentry, there was a retrograde block. Huang et al. performed long-term ECG monitoring. It was found that about one-third of patients had various forms of ventricular tachycardia. The mechanism was mainly due to the increase of catecholamine levels and excessive myocardial muscle fibers. Pulling increases the end-diastolic volume of the ventricle, and patients with hypertrophic cardiomyopathy may have spontaneous or secondary ventricular tachycardia, which may be polymorphic ventricular tachycardia, a few monomorphic ventricular tachycardia, Kuck, Sarage, Marou, etc. Long-term ECG monitoring of patients with ventricular tachycardia was found to be 19% to 50%, which may be characterized by non-sustained or persistent ventricular tachycardia. Continuous ventricular tachycardia may lead to ventricular fibrillation. The direct cause of death of syncope and sudden death, ventricular tachycardia in restrictive cardiomyopathy is more common, the pathological changes are a few millimeters of fibrous thickening in the endocardium and endocardium, intraventricular membrane hardening, often involving the ventricular inflow And apex, and can be extended to the ventricular papillary muscles, chordae, mitral and tricuspid valve posterior lobe, common in tropical and temperate regions, China has only sporadic cases, in cardiomyopathy, there is a so-called heart rhythm Abnormal right ventricular dysplasia (ARVD) of right ventricular cardiomyopathy, based on refractory ventricular tachycardia and right ventricular enlargement, the right chest lead (V1, V2) of the patient's electrocardiogram can be seen with inverted T waves and Diffuse myocardial damage, tachycardia ECG showed left bundle branch block pattern, I lead is R type, ventricular tachycardia originated from right ventricular outflow tract, electric axis is right deviation; ventricular tachycardia originated from right ventricular apex At the bottom of the heart, the motor axis is extremely left-left, and the ventricular arrhythmia is often single-sourced. Some people think that this is the difference between idiopathic ventricular tachycardia and Brugada syndrome.

Coronary heart disease (15%):

Various types of coronary heart disease such as acute myocardial infarction, old myocardial infarction, angina pectoris or painless myocardial ischemia can cause ventricular tachycardia. Acute myocardial ischemia can cause reentry induced by delayed myocardial activation in the ischemic area. Activity, old myocardial infarction is often the reentry of myocardial infarction in the infarct edge scar, the pathological basis of ventricular tachycardia in patients with myocardial infarction, mainly for significant wall motion abnormalities, left ventricular aneurysm formation and significant left Ventricular dysfunction.

Mitral valve prolapse (10%):

Ventricular velocity originates from the breast muscle and annulus, often caused by reentry, mostly monomorphic ventricular tachycardia, and polymorphic ventricular tachycardia is caused by increased self-discipline or triggering activity, which is considered to be the mechanism of sudden cardiac death.

Myocarditis (10%):

Often a common cause of ventricular tachycardia.

Other diseases (5%):

In addition, hypertensive heart disease, valvular heart disease, congenital heart disease, etc. can also cause varying degrees of ventricular tachycardia.

Electrolyte disorders and acid-base balance disorders (10%):

Such as hypokalemia, hyperkalemia, hypomagnesemia and acidosis often cause ventricular tachycardia, if combined with organic heart disease, ventricular tachycardia is more likely to occur.

Drug and toxic effects (10%):

Such as digitalis drugs, anti-cardiac drug quinidine, sympathomimetic drugs, penicillin allergy.

Idiopathic ventricular tachycardia (8%):

Refers to ventricular tachycardia in patients with no obvious organic heart disease, accounting for about 10% (7% to 56%) of the total number of ventricular tachycardia in the majority of young adults, patients may have heart disease, special Hair is relative.

Pathogenesis

1. Foldback mechanism

Reentry means that the impulse returns after activating a segment of myocardial tissue, and once again stimulates the segmental tissue. The formation of the reentry must have a reentry loop, one part of the conduction pathway has a one-way block, and the other part has a slow conduction rate of three conditions. The ventricular premature contraction associated with reentry is usually stable, and the interstitial interval is fixed. The ventricular arrhythmia is mostly caused by the reentry mechanism. It is divided into large reentry and micro-reentry. The reentry caused by ischemic myocardial tissue is a large reentry. The large scar tissue formed after necrosis has no electrical activity and conduction ability, but the complex around the scar tissue and the ischemic myocardium form a complex interweaving, resulting in slow conduction and refractory period, and the circular reentry that can be formed by the movement around the scar tissue. Ventricular arrhythmia, micro-return is the most common reentry in the heart chamber.

2. Trigger activity

The tiggered activity is generated by the posterior depolarization of the myocardial fibers. This post-depolarization can occur during repolarization (early post-depolarization), or after repolarization (late depolarization), after the early stage. The depolarization occurs during the repolarization process, and the late depolarization occurs after the completion of the repolarization or near completion.

(1) Early post-depolarization: After the myocardial action potential rises after the 0 pole, when the pole is not completely repolarized, that is, in the platform phase or the third phase, the membrane potential oscillation reaches the threshold potential, triggering another action potential is the early post-depletion. pole.

(2) Late depolarization: After the late depolarization occurs after the 3-pole repolarization of the action potential is completed, the maximum diastolic potential recovers close to the normal value, which is an oscillation of the membrane potential. When the amplitude reaches the threshold potential, The action potential is generated, that is, the so-called trigger activity, such as the membrane potential oscillation does not reach the threshold potential, which is manifested as the subthreshold posterior depolarization, and the trigger activity is terminated. It has been confirmed that the trigger activity is more and more occupied in the mechanism of ventricular arrhythmia. Important position.

3. Self-discipline enhancement

Self-discipline is determined by diastolic depolarization, rate, threshold potential and maximum diastolic potential, including normal self-regulation and abnormal self-discipline. There are two main reasons for the enhancement: one is the action phase 4-phase depolarization. Enhancement, in myocardial injury, hypoxia, digitalis overdose, hypokalemia and some drug effects can be caused; second, due to the decrease in resting membrane potential.

Elderly ventricular tachycardia prevention

Ventricular tachycardia is a very serious arrhythmia, prevention must be carried out, efforts should be made to find and treat various reversible lesions that induce and maintain ventricular tachycardia, such as ischemia, hypotension and hypokalemia, etc. Decreased to reduce the number of ventricular tachycardia, sinus bradycardia or atrioventricular block, ventricular rate is slow, prone to ventricular tachycardia, can be given atropine treatment, or artificial heart pacing.

Choice of drug prophylaxis: Class I anti-arrhythmia drugs have better effect on inhibiting ventricular rhythm, but can not prevent sudden death, long-term application can increase mortality, can not be used as a preventive drug, class II -blockers inhibit ventricular Arrhythmia is not strong, but it has a significant reduction in mortality, reducing cardiac arrest and sudden death. Class III drugs have antiarrhythmic anti-ventricular ventricular fibrillation, anti-ischemic effects, and prevent sudden death and prolong life. Therefore, prevention Ventricular arrhythmia is effective, its representative is amiodarone, class IV calcium antagonists verapamil and diltiazem are effective in preventing verapamil sensitive ventricular tachycardia, antiarrhythmic drugs can be combined with buried ventricles or atrium The device is combined to treat ventricular tachycardia.

Drug treatment options: Amiodarone is a benzofuran microorganism, a broad-spectrum antiarrhythmic drug, especially for the treatment of malignant arrhythmias.

Complications of ventricular tachycardia in the elderly Complications

There may be syncope, ventricular fibrillation, sudden cardiac death and so on.

Symptoms of ventricular tachycardia in the elderly Common symptoms Ventricular fibrillation separation of sudden cardiac arrhythmia Head or neck bloating and beating heart muscle infarction palpitations Hemorrhoids tachycardia ventricular flutter

Clinical manifestation

(1) Symptoms: The clinical manifestations of ventricular tachycardia are not consistent.

1 Symptoms: There may be palpitation, chest tightness, chest pain, black Mongolian, syncope, and its clinical features are sudden onset, sudden disappearance after treatment or self-limiting, sudden palpitations, rapid heart rate, mental anxiety, fear, pre-heart Area discomfort, head or neck bloating and jumping.

2 Asymptomatic: People with non-sustained ventricular tachycardia are usually asymptomatic and are only found in physical examinations or 24h ambulatory electrocardiograms.

(2) Signs: auscultation heart rate is mild and irregular, first, two heart sounds split, systolic blood pressure can change with heart beat, such as complete atrioventricular separation, the first heart sound intensity often changes, the jugular vein intermittently appears huge a Wave, when the ventricle beats back and continues to capture the atria, the atrium and the ventricle contract at almost the same time, the jugular vein presents a regular and huge a wave.

2. Classification

Classified according to the way of attack.

(1) Paroxysmal ventricular tachycardia, also known as pre-systolic ventricular tachycardia, refers to ventricular tachycardia composed of three or more ventricular premature contractions, often Excited for a ventricular premature contraction, if sustained for more than 30s is called persistent ventricular tachycardia; seizure <30s, called non-sustained ventricular tachycardia, recurrent ventricular tachycardia, only 1 ~ 2 sinus beat intervals, called recurrent ventricular tachycardia, and its ECG features:

1 consecutive ventricular premature contractions of 3 or more times, QRS complex broad deformity, time > 0.12 s, and secondary ST-T changes.

2 The frequency is 120-180 times/min. If it is less than 110 times/min, it is called non-paroxysmal ventricular tachycardia. If the heart rate is more than 200 times, the sinusoidal wave appears as ventricular pulsation.

There is no constant P wave before the 3QRS complex, that is, there is no fixed relationship between the P wave and the QRS complex.

4 heart rhythm rules or mild irregular RR interval difference <0.03s.

5 When tachycardia occurs, ventricular capture or ventricular fusion waves may occur.

6-ventricular tachycardia showed a sudden onset and abrupt termination.

According to the ECS QRS complex, paroxysmal ventricular tachycardia is further divided into monomorphic ventricular tachycardia, polymorphic ventricular tachycardia and bidirectional ventricular tachycardia.

Polymorphic ventricular tachycardia refers to the presence of three or more forms of QRS complexes on the same lead of the electrocardiogram in the onset of tachycardia. There are two types: 1 tip torsade ventricular tachycardia : Before the onset of tachycardia, the QT interval is prolonged. When the tachycardia occurs, the QRS complex is twisted up and down along a baseline. The QRS amplitude is sinusoidal in each cycle, and its pathophysiological changes: early Dessertenae proposed, intraventricular There are two competitive cardiac excitatory points alternately controlling the ventricle. Later, some scholars believe that the QT is prolonged due to the reentry mechanism, and the ventricular repolarization is inconsistent. Therefore, there is a formation of reentry, but some scholars have found that pacing cannot be induced. Recently, some animal experiments have shown that due to the increased self-discipline of ectopic excitatory points in the heart, 2 polymorphic ventricular tachycardia: normal QT interval before the onset of tachycardia, when the tachycardia occurs, the electrocardiogram is the same There are three or more QRS complexes on the joint (Figure 1).

Bidirectional ventricular tachycardia, clinically rare, is common in severe organic heart disease, such as dilated cardiomyopathy, coronary heart disease or digitalis poisoning patients, the patient's basic rhythm is often atrial fibrillation, refers to ventricular cardiac motility In the case of a rapid attack, the positive and negative changes of the main wave direction of the QRS complex on the same lead of the electrocardiogram may occur as follows:

1 Indoor two pacemakers alternately give excitement.

2 single-source ventricular tachycardia with alternating indoor difference transmission.

3 One pace point is indoors and the other pace point is located on the chamber.

When the ventricle is transmitted under the 4th room, the alternating conduction of the left and right bundle branches and their branches occurs.

(2) non-paroxysmal ventricular tachycardia, also known as accelerated ventricular arrhythmia, slow ventricular tachycardia, ventricular self-pacing tachycardia, etc., refers to the ectopic rhythm point self-discipline in the ventricle Increased sexuality, close to or slightly exceed the self-discipline of sinus pacemakers, and a tachycardia that temporarily controls the ventricle, more common in more serious structural heart disease, such as coronary heart disease, myocardial infarction, ventricular aneurysm, Cardiomyopathy, etc., as well as digitalis drug poisoning or electrolyte imbalance, the characteristics of the electrocardiogram are:

1 rhythm rule, heart rate is 60 ~ 100 times / min.

The 2QRS wave group appears three or more consecutively, and there is no constant P wave before it.

3QRS wave group wide deformity.

4 visible ventricular capture or ventricular fusion wave.

Retrograde P waves can be seen after 5 partial QRS complexes.

6 ventricular tachycardia can alternate with sinus rhythm.

Classification of hemodynamics and prognosis based on ventricular tachycardia:

1 Benign ventricular tachycardia, clinical evidence of organic heart disease, no obvious hemodynamic disorder during ventricular tachycardia, no obvious palpitation for hours or days Symptoms such as chest tightness, mostly idiopathic ventricular tachycardia or short-term ventricular tachycardia, normal idiopathic ventricular tachycardia, most of the prognosis is good, but there are obvious symptoms at the time of onset, when drug treatment is invalid, Radiofrequency ablation can be used.

2 potential malignant ventricular tachycardia, such arrhythmia occurs on the basis of a clear structural heart disease, common in patients after myocardial infarction and patients with cardiomyopathy, ventricular tachycardia may have Symptoms such as palpitation and chest tightness may also have no symptoms directly related to them. Such arrhythmia may have independent prognostic significance, and the treatment target is mainly aimed at improving the prognosis.

3 malignant ventricular tachycardia, almost all have hemodynamic performance and signs, there are obvious clinical symptoms at the time of attack, such as palpitation, chest tightness, syncope, etc., with a high risk of sudden cardiac death, common are:

A. Survivors with no evidence of infarction and sudden recovery from the outpatients, mostly patients with coronary heart disease.

B. Infarct or dilated cardiomyopathy combined with monomorphic persistent ventricular tachycardia.

C. Idiopathic ventricular fibrillation, with a genetic predisposition, found in children or youth.

D. Brugada syndrome, ECG performance: normal QT interval, right bundle branch block and right chest lead (V1 ~ V2) ST segment sustained elevation, cardiac ultrasound, ventricular angiography or even myocardial biopsy heart no abnormal changes A syndrome that is more common in young and healthy people.

Examination of ventricular tachycardia in the elderly

Patients with no structural heart disease should check blood, potassium, magnesium, pH and so on. The electrocardiogram shows the characteristics of a typical ventricular tachycardia.

Diagnosis and diagnosis of ventricular tachycardia in the elderly

Diagnostic criteria

Electrocardiogram

It is a reliable method for diagnosing ventricular tachycardia. The main basis is:

1 Wide and malformed QRS complex with a time limit of >0.12s and more than three consecutive occurrences.

2 heart rate > 120 times / min.

3 compartments were separated, and ventricular rate > atrial rate.

4 have ventricular capture or ventricular fusion waves.

5 If the shape of the QRS complex is monomorphic, the rhythm is basically regular. Generally, the RR interval is less than 20ms. Even if there is slight unevenness, the difference between the RR intervals is more than 20~30ms, and the ECG is for ventricular. The tachycardia not only has qualitative value, but also can roughly determine the location of the origin point according to the morphological characteristics of the QRS complex. The accuracy of the initial positioning can reach more than 80%, and the QRS complex of the tachycardia is the right bundle. In patients with retardation, tachycardia originates from the left ventricle; the QRS complex of tachycardia is left bundle branch block, tachycardia originates from the right ventricle; II, III, avF leads the main wave upward, heartbeat The overspeed originates from the outflow tract or the base; the II, III, avF leads the main wave to the lower, the tachycardia mostly originates from the septum or apex, and the V1 to V6 leads the main wave to the upper, the tachycardia originates from The posterior wall of the ventricle; the main wave of the V1 ~ V6 lead is lower, and the tachycardia originates from the anterior wall of the ventricle.

2. Dynamic ECG

For tachycardia that is difficult to detect with conventional ECG, dynamic electrocardiography should be performed, especially for patients with recurrent episodes of syncope. Dynamic electrocardiography is more meaningful, including:

1 determine the presence or absence of ventricular tachycardia;

2 understand the changes in ventricular tachycardia;

3 to understand the relationship between ventricular tachycardia and clinical manifestations;

4 understand the combined arrhythmia and ST segment changes;

5 evaluate the effect of antiarrhythmic drug treatment.

3. Cardiac electrophysiological examination

Cardiac electrophysiological examination has a great diagnostic value for ventricular tachycardia. If the His bundle potential (H) can be recorded at the onset of tachycardia, the Hess bundle potential is analyzed to the ventricular potential (V). The initial interval (HV interval) is helpful for the identification of supraventricular tachycardia and ventricular tachycardia. Application of electrical stimulation technique, about 95% of patients with persistent monomorphic ventricular tachycardia induce the same clinical ventricular tachycardia, crown Ventricular tachycardia and persistent ventricular tachycardia are more likely to be induced than non-sustained ventricular tachycardia, non-sustained ventricular tachycardia, and programmed electrical stimulation or rapid pacing can terminate 75% of persistent monomorphic ventricular tachycardia. A 25% ventricular tachycardia requires DC conversion.

Differential diagnosis

1. With supraventricular tachycardia (referred to as supraventricular tachycardia)

Identification of the QRS complex (the original bundle branch block):

(1) When the supraventricular velocity is accompanied by the left bundle branch or the right bundle branch block, the wide QRS waveform should show a typical bundle branch block pattern. For example, when the supraventricular bundle is accompanied by the left bundle block, the electric axis should be left-biased, V1 V2 lead is rS type, r wave interval should be <30ms, V5, V6 lead should not appear q wave, etc., previous ECG or restorative sinus rhythm ECG on supraventricular tachycardia with original bundle branch block Diagnosis is important.

(2) It is difficult to distinguish between supraventricular velocity and continuous ventricular tachycardia. The occurrence of differential conduction may be a functional change of the indoor bundle branch or a pathological change. The right bundle branch block type Most of the features, right bundle branch block or left bundle branch block is common in patients with cardiac organic disease.

2. Identification of retrograde atrioventricular reentry tachycardia

Reverse-type atrioventricular reentry tachycardia, that is, atrioventricular reentry tachycardia through the atrioventricular bypass, atrial activation through the atrioventricular bypass, ventricle, and ventricular activation from the atrioventricular node, retrograde atrial, ventricular Excited by the bypass, the QRS wave is wide and deformed, and its frequency is above 220 beats/min, while the frequency of ventricular tachycardia is more than 100-220 beats/min. It is rare for more than 220 beats/min. .

3. Identification of pre-excitation syndrome (pre-excitation) with atrial fibrillation

(1) When atrial fibrillation occurs in pre-excitation syndrome, a wide-sex malformed QRS wave tachycardia occurs, but there is also a narrow QRS complex or ventricular fusion wave, which causes changes in the shape of the QRS before and after the ECG.

(2) When atrial fibrillation is combined with pre-excitation, the P-wave disappears due to the basal heart rhythm, and the RR interval is absolutely different. After restoring sinus rhythm, the ECG can see the pre-shock.

(3) Atrial fibrillation combined with WPW syndrome, atrial fibrillation is often caused by room reentry, after ablation bypass treatment, most patients no longer have atrial fibrillation.

4. History and clinical manifestations identify ventricular tachycardia and other wide QRS tachycardia

(1) In general, there is a history of organic heart disease, especially in patients with acute myocardial infarction, the wide QRS wave tachycardia should be considered first, in patients with no structural heart disease, recurrent Most of the tachycardia is the speed of the room.

(2) Stimulation of the vagus nerve, including carotid sinus massage, pharyngeal stimulation, pressing the eyeball, etc., can terminate the wide QRS wave tachycardia, then consider the supraventricular tachycardia.

(3) Wide QRS wave tachycardia episodes, such as accompanied by more obvious hemodynamic disorders, such as severe chest tightness, blood pressure, angina, and even A-S syndrome, mostly ventricular tachycardia, a few frequencies Rapid room velocities can also have hemodynamic changes, but rarely cause A-S syndrome.

The diagnosis of ventricular tachycardia is mainly based on symptoms, signs, electrocardiogram, 24h dynamic electrocardiogram, etc., because of its variety, there are single, multiple, polymorphic, multi-source, pair and ventricular tachycardia, whether it is related to different causes Symptoms and hemodynamic disorders, whether it needs treatment and prognosis, there are currently advocated classification, one is benign ventricular arrhythmia, such as multi-organic heart disease, good prognosis, and second, prognostic heart rhythm Abnormalities exist on the basis of obvious organic heart disease, the treatment target is mainly for the improvement of prognosis, and the third is the poor prognosis of malignant ventricular arrhythmia, and ICD is required.

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