Intermittent-dependent torsades de pointes ventricular tachycardia

Introduction to intermittent dependent torsade ventricular tachycardia Intermittent-dependent torsade ventricular tachycardia (pausedependenttorsades despointesventriculartachycardia, PTDPVT) often occurs in older patients due to certain medications, electrolyte imbalance (low potassium, low magnesium, low calcium) and obvious causes for various reasons Bradycardia, some organic heart disease, etc. lead to prolonged QT interval, causing torsade ventricular tachycardia. basic knowledge The proportion of sickness: 0.003%-0.005% Susceptible people: no special people Mode of infection: non-infectious Complications: syncope, A-S syndrome, sudden death

Intermittent-dependent torsade-type ventricular tachycardia

What is the cause of intermittent-dependent torsade-type ventricular tachycardia?

(1) Causes of the disease

1. Drug causes LQTS

(1) antiarrhythmic drugs: such as quinine IA, procainamide, diisopropylpyramine; IB class of lidocaine, mexiletine may have a role in promoting TDP; IC class Enkani Propafenone can induce TDP; class II sotalol, Senatilide can cause TDP (> 5%) due to prolongation of QT interval; class III amiodarone; class IV bepridil can cause TDP.

(2) Drugs for the treatment of psychosis: such as phenothiazine, fluridol, tricyclic and tetracyclic anti-inhibitors.

(3) Other drugs: antihypertensive drugs, lidofluzine, erythromycin, antihistamine preparations, ketoconazole, astemizole, amantadine, organophosphorus pesticides, arsenic, lithium, etc., drug cocaine Can lead to prolonged QT interval.

2. Electrolyte abnormalities

(1) hypokalemia: can cause an increase in the U wave of the electrocardiogram, prolonging the QT or QTU interval.

(2) hypomagnesemia: often accompanied by hypokalemia.

(3) Hypocalcemia.

3. Severe bradycardia can be seen in high or complete atrioventricular block, sinus arrest, severe sinus bradycardia, sick sinus syndrome, atrial fibrillation, long RR interval, etc., atrioventricular block Studies have shown that it is not the bradycardia itself that causes TDP, but the pathological QT interval prolongation and repolarization abnormalities due to heart rate changes.

4. The impact of heart disease on QT interval Myocardial ischemia, hypoxia, myocardial infarction, myocarditis, cardiac tumor, cardiac insufficiency, etc. can cause QT interval prolongation.

5. Central nervous system diseases, brain trauma, encephalitis, cerebrovascular accidents, etc.

6. Endocrine disease hypothyroidism, hyperthyroidism, hyperaldosteronism.

7. Malnutrition hunger (such as neuropathic appetite), liquid protein diet.

8. Unexplained LQTS is rare and difficult to identify.

(two) pathogenesis

Various causes cause cell membrane ion channel dysfunction and lead to prolongation of QT interval. The concurrent TDP often starts in long and short order and intermittently dependent form. The mechanism of TDP formation is driven by factors such as drugs and electrolyte abnormalities. The current increases, the repolarization delays, and the depolarization occurs especially after the early depolarization forms an oscillating current. Once the threshold is reached, the triggering arrhythmia can be triggered, and the significant period of bradycardia can block or completely lose the potassium channel. Live, but the potassium ion outwards decrease or disappear, actually increase the inward current, which can promote TDP, which is due to the long compensatory interval caused by the short-term inter-temporal contraction , or severe bradycardia, long intermittent after paroxysmal tachycardia, and atrial fibrillation long RR interval, so called long interval-dependent TDP.

QT interval prolongation of torsade ventricular tachycardia is mostly induced by ventricular premature contraction (R-on-T). In a few cases, atrial premature contraction is also one of the trigger factors, ventricular myocardium atrial Depolarization caused by pre-contraction will aggravate the original repolarization inhomogeneity and induce TDP.

Intermittent-dependent torsade-type ventricular tachycardia prevention

In addition to avoiding or actively treating the factors that cause the prolongation of QT interval, it is necessary to timely understand the drug use and changes in the condition of the drug, and find out the situation in a timely manner, which can effectively prevent its occurrence.

When using drugs that can cause prolongation of QT interval, ECG changes should be closely observed. If the QT interval is >0.50s or the extended value after administration exceeds 25% before administration, the drug should be stopped immediately to prevent hypokalemia and hypokalemia. Magnesium; and should avoid the combination of IA and II, III antiarrhythmic drugs.

Intermittent-dependent torsade ventricular tachycardia complications Complications syncope A-S syndrome sudden death

Intermittent-dependent torsional ventricular tachycardia may have syncope and convulsions when the attack time is long due to hemodynamic effects. Even complications such as A-S syndrome and sudden cardiac death may occur. The most prominent manifestation of A-S syndrome is sudden fainting. The lighter ones are only dizzy, loss of consciousness, and complete loss of consciousness. Often accompanied by convulsions and incontinence, pale, and then bruising, there may be snoring and wheezing breathing, sometimes see Chen Shi's breathing.

Intermittent-dependent torsade-type ventricular tachycardia symptoms Common symptoms tachycardia, dizziness, dizziness, chest tightness, ventricular fibrillation, ventricular flutter, convulsions, heart palpitations

What are the manifestations and how to diagnose intermittently-dependent torsade-type ventricular tachycardia?

Ventricular tachycardia may have palpitations, chest tightness, dizziness and other symptoms. The longer duration of seizures may cause short-term syncope and convulsions. Although the seizures may terminate spontaneously, they are easily recurrent and evolve into ventricular flutter. Movement, ventricular fibrillation, can easily lead to hemodynamic disorders, it must be actively treated, complete control of seizures in a short period of time, most of the seizures have no obvious symptoms, may have ventricular premature contractions, bradycardia, etc. There are symptoms of the primary disease.

Patients often have seizures, for example, history of antiarrhythmic drugs, hypokalemia, hypomagnesemia, history of bradycardia, history of QT prolongation of electrocardiogram, etc., which occur within a few days after taking the drug. The dose and blood concentration of the drug were normal or low, and some had a history of frightening or emotional induction, and the family history was negative.

This type of ventricular tachycardia is between pathological paroxysmal ventricular tachycardia and ventricular fibrillation, and the cardiac output is significantly reduced, so it is prone to repeated syncope, A-S syndrome, short-lived less than 4s. Ventricular tachycardia is generally only palpitations, dizziness, if it lasts for more than 5s, it is prone to syncope and convulsions.

1. Electrocardiogram features tachycardia characterized by torsades de point ventricular tachycardia, QT interval prolonged, T, U changes, long-short circumference, R-on-T bimodal ventricular premature contraction induced long Intermittent-dependent TDP, the onset of more than 3 to 5 s, can terminate spontaneously, but repeated attacks.

2. There are clear causes.

Intermittent-dependent torsade-type ventricular tachycardia

What should be done for intermittently dependent torsade ventricular tachycardia?

1. ECG examination features

(1) Intermittent-dependent torsional ventricular tachycardia typical ECG features:

1 pre-existing ventricular premature contraction: often begins with R-on-T type ventricular premature contraction, or induced by late diastolic ventricular premature contraction of R on U waves (Fig. 1).

2 There were a series of large and abnormal malformed QRS complexes with different amplitudes at different episodes. The frequency of ventricular tachycardia was 180-260 beats/min, with an average of 220 beats/min, and the individual reached 310 beats/min. At the time of the attack, the frequency gradually accelerated, and gradually slowed down and the amplitude became larger before the termination. The QRS waveform and duration variation of each episode was variable, often accompanied by RR spacing changes (Fig. 2).

3 The polarity and amplitude of the QRS complex showed a phase change at the time of attack: the main wave direction of the QRS wave every 5-20 beats was abruptly or gradually turned to the opposite direction around the baseline, showing a spindle shape (Fig. 3).

4 The onset time is generally shorter: it lasts from a few seconds to more than ten seconds, or tens of seconds, even longer (there is a report lasting 6 minutes), and the termination occurs when the basic rhythm occurs after an interval of different lengths (Fig. 1), or by A form and direction of the QRS complex between the basic heart rhythm and the ectopic heart rhythm, and then transition to the basic heart rhythm.

5 Although it can be terminated by itself to sinus rhythm: but it is easy to recurrent, if not active treatment can be converted into ventricular flutter, ventricular fibrillation (Figure 4).

(2) Typical ECG characteristics of intermittent TDP episodes:

1 The basic heart rhythm is mostly slow arrhythmia: such as sinus bradycardia, junctional heart rhythm, high or complete atrioventricular block, occasional second degree atrioventricular block, pre-systolic contraction, intermittent atrial The tremor RR long interval, etc., can also be normal sinus rhythm (Figure 5).

2 The QT or QTu interval of the basic heart rhythm is significantly prolonged (can exceed 0.60 s) (Fig. 6).

3T wave widening, low level or inverted: U wave is obvious, it can also be wide, polymorphous, etc., often combined with T wave, U wave system caused by repolarization abnormality, the longer the interval, the more obvious U wave.

4-ventricular tachycardia is often induced by a ventricular premature contraction with a longer inter-term interval. The inter-term interval is usually 0.5-0.7 s, and can even be induced by atrial pre-contraction.

5 visible ventricular premature contraction: frequent, often R-on-T, R-on-U phenomenon, TDP attacks often start with R-on-T ventricular pre-contraction dichotomy, due to QT The period is significantly prolonged, so the R-on-T ventricular premature contraction often has a longer inter-term interval, which is obviously different from the short-term interval between the general R-on-T ventricular pre-contraction, so it is called Special two-law (Figure 7).

6 A few minutes before the onset of TDP, several hours or intermittent periods, sometimes high (or deep) additional waves appear at the top or end of the T wave, in addition to atrial fibrillation, in the II, III, aVF leads and left The T-wave end of the chest lead, that is, the Dows wave (slow wave) appears at the traditional U wave. In each direction of the lead and the T wave (Fig. 8), the patient's Dows wave also has an alternating voltage.

(3) A detailed description of a typical ECG of intermittently dependent TDP:

1 The cycle of the cardiac cycle: 90% to 98% of patients in the last sinus (or supraventricular) heartbeat before the onset of TDP, before the long RR interval is a long cycle (such as bradycardia or pre-term Long interval after contraction or RR interval of atrial fibrillation, etc., and ventricular premature contraction that promotes ventricular tachycardia (ie, R-on-T or R-on-U ventricular premature contraction) On the TU wave of the QT interval in which the previous sinus (or supraventricular) pulsation is prolonged (ie, the interphase interval of ventricular premature contraction, that is, the short period), thereby forming a long cardiac cycle during the onset of TDP A short interval (also known as long-short circumference) induces regular changes.

When 2 ventricular tachycardia continues to attack: QRS wave shape is tip-twisted, pleomorphic, and very few can be converted into monomorphic ventricular tachycardia. The frequency of short-term attacks is relatively slow and the shape is single, so only in many cases Leads and long-term records show its characteristics.

3 ventricular frequency: Because the distance between QRS waves is not equal, it is often difficult to accurately measure, so the frequency range is reported differently, such as report 180 ~ 260 times / min, 120 ~ 360 times / min, etc., the upper limit of this type of TDP frequency and ventricle Flutter or ventricular fibrillation overlap, the lower limit overlaps with pathological paroxysmal ventricular tachycardia, the fast phase and slow phase of QRS wave can be distinguished, and ventricular fibrillation can not be distinguished. Most TDP frequencies are fast and have a cycle. Sexual seizure tendency, once attacked for a while, then repeated episodes and gradually continued, and even developed into ventricular fibrillation and died.

4T wave and U wave: In the TDP, the shape and amplitude of the T wave are alternated and/or T wave deformation is common. The U wave shape amplitude can periodically fluctuate after the interval, that is, from large to small, from small to large. The faster the ventricular rate before the interval, the longer the interval time, the more obvious the U wave, the faster the TDP frequency, the longer the duration, the longer the attack time, the more diverse the shape, and the TDP attack is related to the U wave, which is typical. The amplitude of the U wave increases exponentially. When a certain height (threshold) is reached, TDP is triggered. It is called the slow wave is the starting factor of the TDP attack. It often starts at the peak or descending branch of the U wave, U wave. Often in the left chest lead is obvious, in the II, V5 lead erect, wide or double peak, T wave can be inverted two-way, U wave can be greater than T wave, there are no U wave (about 10%).

5Q-T interval, Q-Tc interval: almost all patients were significantly prolonged, Q-Tc interval was 0.46 ~ 0.56s.

6TDP can be converted by itself: this is a major feature, but it is easy to recurrent and must be treated before it can finally terminate the recurrence of TDP.

7TDP episode duration and intermittent time: usually the episode duration is shorter, mostly in the seconds to tens of seconds, mostly lasting 3 to 5s, but also up to 22s, even lasting 6min, the interval period is uncertain, the short is only 1~2s, repeated The author's interval is usually shorter.

2. Electrophysiological examination features

(1) Recording the right ventricular endocardial single-phase action potential with the Franz contact electrode: The early post-depolarization can be recorded, located in the single-phase action potential repolarization phase 3, and occurs synchronously with the surface electrocardiogram U wave.

(2) Ventricular stimulation and frequency-increasing stimulation (or intravenous infusion of isoproterenol: 2 g/min) failed to induce ventricular tachycardia.

(3) rapid pacing of the right ventricle: 10s each time, showing the QTU interval and U wave amplitude changes caused by sudden deceleration after rapid pacing, and positively correlated with intermittent length and pacing frequency.

Diagnosis and diagnosis of intermittent dependent torsade ventricular tachycardia

What are the diseases that intermittent-dependent torsade-type ventricular tachycardia are easily confused with?

Distortion of torsade ventricular tachycardia and other polymorphic ventricular tachycardia is difficult, mainly based on the prolongation of QT interval, U wave, often no serious organic heart disease, have a special cause, often recurrent and Can be terminated by itself.

1. Need to be differentiated from general ventricular tachycardia or ventricular fibrillation. The general ventricular tachycardia is characterized by a series of broadly fixed wide QRS waves. The ST segment and T wave can be identified, often do not stop by themselves; the general ventricular tachycardia can also be early by RonT room. Induced, but the interval between the early chambers is short, the QRS wave and the ST segment and the T wave cannot be recognized during ventricular fibrillation. The ventricular rate is greater than 300 times/min, which is extremely irregular. Generally, it does not terminate spontaneously. The electric shock cardioversion is effective and the QRS wave of TDP is effective. It is identifiable with ST-T, and the ventricular rate is more than 200 times/min. The duration of the attack is short and will terminate spontaneously, but it can be repeated and the effect of electric shock cardioversion is poor.

2. Need to distinguish from other polymorphic ventricular tachycardia and ventricular fibrillation The following two points are helpful for differential diagnosis:

On the electrocardiogram before or just after the onset of ventricular tachycardia, if there is a prolongation of the QT interval and the presence of U waves, a relatively long interphase interval, or a typical induction sequence (long one short circumference), Then support TDP;

The clinical situation when 2-ventricular tachycardia occurs is helpful for differential diagnosis.

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