Overview.
Intermittent dependent tip-twisting ventricular tachycardia (PTDPVT) often occurs in older patients with tip-twisting ventricular tachycardia (TDP) due to prolongation of the Q-T interval as a result of the administration of certain medications, electrolyte disturbances (low potassium, low magnesium, low calcium) and significant bradycardia due to various causes, certain organic heart diseases, and other causes.
Etiology
1. Drug-induced LQTS
(1) Antiarrhythmic drugs, such as quinidine, procainamide, bis-isopropylpyrimethamine of class IA; lidocaine and mexiletine of class IB may have the effect of triggering TDP; Encarnitine and propafenone of class IC may occasionally induce TDP; sotalol and Senatilide of class II may prolong the Q-T interval and cause TDP (> 5%); amiodarone of class III; and bepridil of class IV may cause TDP.
(2) Drugs for the treatment of psychosis, such as phenothiazine, flupentixol, tricyclic and tetracyclic antidepressants.
(3) Other drugs Antihypertensives, ritoflurane, erythromycin, antihistamines, ketoconazole, astemizole, amantadine, organophosphorus pesticides, arsenic, lithium, etc., and the drug cocaine can also lead to prolongation of the Q-T interval.
2. Electrolyte abnormalities
(1) Hypokalemia can lead to increased U wave on ECG and prolonged QT or Q-T-U interval.
(2) Hypomagnesemia is often accompanied by hypokalemia.
(3) Hypocalcemia
3. Severe bradycardia
Severe bradycardia can be seen in high or complete atrioventricular block, sinus arrest, severe sinus bradycardia, pathological sinus node syndrome, atrial fibrillation with long R-R intervals, etc. Studies of atrioventricular block have shown that it is not the bradycardia per se that contributes to the development of TDP, but rather the pathologic prolongation of Q-T intervals and the abnormalities of repolarization due to changes in heart rate.
4. Effects of cardiac diseases on Q-T interval
Myocardial ischemia, hypoxia, myocardial infarction, myocarditis, cardiac tumor, cardiac insufficiency, etc. can cause Q-T interval prolongation.
5.Central nervous system diseases
Traumatic brain injury, encephalitis, cerebrovascular accident, etc.
6. Endocrine diseases
Hypothyroidism, hyperthyroidism, aldosteronism.
7. Malnutrition
Starvation (e.g., neurogenic lack of appetite), liquid protein diet.
8. Unexplained LQTS
Rare and difficult to identify.
Symptoms
Ventricular tachycardia may have palpitations, chest tightness, dizziness, etc., the attack lasts for a long time may cause short-term syncope and convulsions, although the attack can be terminated on its own, but it is very easy to have recurrent attacks, and there is a possibility of evolving into ventricular flutter, ventricular fibrillation, which can easily lead to hemodynamic disorders, so it is necessary to treat it actively, and to control the attack completely within a short time, and the majority of the symptoms are not obvious during the interictal period, and there can be ventricular pre-ejection and bradycardia, etc., and there are primary diseases. The symptoms of the primary disease may be present, such as ventricular pre-systole, bradycardia, and so on.
This type of ventricular tachycardia is intermediate between pathologic paroxysmal ventricular tachycardia and ventricular fibrillation, and the decrease of cardiac output is more obvious, so it is prone to recurrent syncope, A.S. syndrome, and the transient ventricular tachycardia less than 4 seconds usually only has palpitation and dizziness, but if it lasts for more than 5 seconds, it is very easy to have fainting and convulsions.
Examination
1. Characteristics of electrocardiography
(1) Typical electrocardiogram of intermittent-dependent torsional ventricular tachycardia (1) Before the onset of the attack, there is ventricular pre-systole, which often starts as R-on-T ventricular pre-systole or is induced by late diastolic ventricular pre-systole with the R falling on the U wave. The frequency of ventricular tachycardia is 180-260 beats per minute, with an average of 220 beats per minute and up to 310 beats per minute. The frequency is gradually accelerated during the onset of tachycardia, and then gradually slowed down before the termination of tachycardia, and the amplitude of the tachycardia becomes larger, and the QRS waveforms and duration of each episode are variable, and are often accompanied by changes in the R-R spacing. The QRS waveform and duration of each seizure are variable, often accompanied by changes in R-R spacing. The polarity and amplitude of the QRS wave group during the seizure show temporal changes: the main wave direction of the QRS wave of every 5-20 beats is suddenly or gradually reversed to the opposite direction around the baseline, which is manifested as a spindle shape. ④ Episode duration: generally short, lasting a few seconds to more than ten seconds, or tens of seconds, occasionally longer (reported to last 6 minutes), the termination of which is characterized by the emergence of the basal rhythm after intervals of varying lengths, or the transition to the basal rhythm by a cluster of QRS waves with a morphology and direction intermediate between the basal rhythm and the ectopic rhythm. ⑤ Regression: Although it can be terminated to sinus rhythm by itself, it is very easy to recur, and if not actively treated, it can be transformed into ventricular flutter and ventricular fibrillation.
(2) Typical electrocardiogram during TDP episodes (1) The underlying rhythm is mostly slow arrhythmia, such as sinus bradycardia, intersectional rhythm, high or complete atrioventricular block, occasionally second-degree atrioventricular block, compensatory intervals after preterm systole, and long R-R intervals of atrial fibrillation, etc., and it can also be normal sinus rhythm. Q-T or Q-T-u interval of the base rhythm is significantly prolonged (more than 0.60 seconds). (iii) T-wave is widened, flattened or inverted, and U-wave is obvious, or it can be broad, polygonal and other changes, often fused with T-wave, and U-wave is the repolarization abnormality caused by the intervals, and the longer the intervals are, the more obvious the U-wave is. Ventricular tachycardia is often induced by a ventricular pre-systole with a long inter-rhythmic interval, which is often 0.5-0.7 seconds, and occasionally by an atrial pre-systole. ⑤ Ventricular pre-systole can be seen as frequent, often R-on-T, R-on-U phenomenon, TDP episodes often start with R-on-T ventricular pre-systolic dysthymia, due to the significant prolongation of the Q-T interval, so the R-on-T ventricular pre-systole often has a longer inter-rhythmic interval, which is different from the short inter-rhythmic intervals of general R-on-T ventricular pre-systolic, and therefore called a special dysthymia. (6) Minutes, hours or intervals before the onset of TDP, higher (or deeper) additional waves can sometimes be seen at the peak or terminal portion of the T wave. In addition to atrial fibrillation, Dows waves (slow waves) appear at the terminal portion of the T wave, i.e., at the traditional U wave, in leads II, III, and aVF, as well as in the left thoracic lead; in each lead, in the same direction as the T wave, the patient’s Dows waves also show alternating voltages.
(3) Typical electrocardiogram of interval-dependent TDP ①Pattern of cardiac cycle: The last sinus (or supraventricular) beat before the onset of TDP is preceded by long R-R intervals, i.e., long cycles (e.g., long intervals after bradycardia or preterm systole, or long R-R intervals in atrial fibrillation, etc.), and ventricular preterm contractions that precipitate ventricular tachycardia (i.e., R-on-T or R On-U ventricular pre-systole) falls on the TU wave of the Q-T interval of the previous sinus (or supraventricular) beat (i.e., the coupled intervals of ventricular pre-systole, i.e., the short period), resulting in a regular change in the cardiac cycle induced by one long and one short interval (also known as a long-short perimeter) during the onset of TDP. ② ventricular tachycardia: continuous episodes of QRS wave morphology is tip-twisted, polymorphic, and rarely can be transformed into monomorphic ventricular tachycardia short burst episodes of frequency is relatively slow, the morphology of a single, so only in the multi-lead and a long time to record to show its characteristics. (iii) Ventricular frequency: It is often difficult to measure accurately because of the unequal distances between QRS waves, so the frequency range is reported differently, such as 180-260 beats/min, 120-360 beats/min, etc. The upper limit of this type of TDP frequency overlaps with ventricular flutter or ventricular fibrillation, and the lower limit overlaps with pathologic paroxysmal ventricular tachycardia, and the fast and slow phases of the QRS wave can be differentiated, while ventricular fibrillation can not be QRS wave fast phase and slow phase can be distinguished, while ventricular fibrillation can not be distinguished, the majority of TDP frequency is fast, and there is a tendency to periodic episodes, once a burst of episodes, and then repeated paroxysms and gradually become persistent, and even develop into ventricular fibrillation and death. T wave and U wave: in TDP, alternating shape and amplitude of T wave and/or deformation of T wave are common; the amplitude of U wave pattern can fluctuate periodically after the interval, i.e., from big to small, from small to big; the faster the ventricular rate before the interval and the longer the interval, the more obvious the U wave is; the faster the frequency of TDP, the longer the duration of TDP, and the longer the duration of the attack, and the morphology can be diversified, and the onset of TDP is correlated with the U wave, typical cases can see U wave amplitude increasing by the minute, and the U wave can be seen as a result of the change in the frequency. Typically, the amplitude of U wave increases by beat, and when it reaches a certain height (threshold), it triggers the occurrence of TDP, which is called slow wave and is the initiating factor of TDP, which often starts at the peak or descending branch of U wave. U wave is often obvious in the left anterior thoracic lead, and it is upright, broad or bimodal in the II and V5 leads, and the T wave is inverted and bi-directional, and the U wave can be larger than the T wave, and there are also cases in which the U wave does not appear (about 1O%). ⑤ Q-T interval: Q-Tc interval is significantly prolonged in almost all patients, and Q-Tc interval is mostly 0.46-0.56 seconds. ⑥ TDP can turn around on its own: this is a major feature, but it is prone to recurrent episodes and must be treated to finally terminate recurrent TDP episodes. (7) The duration of TDP episodes and intervals: usually the duration of the episodes is short, mostly in a few seconds to tens of seconds, mostly lasting 3-5 seconds, but also up to 22 seconds, or even lasting for 6 minutes, the duration of the intervals is variable, the shorter one is only 1-2 seconds, and the intervals of the recurrent episodes are usually shorter.
2. Characteristics of electrophysiologic examination
(1) The monophasic action potential of the endocardium of the right ventricle recorded by Franz contact electrode can be recorded to the early posterior depolarization, which is located in phase 3 of the repolarization of the monophasic action potential and occurs in synchrony with the U wave of the surface ECG.
(2) Ventricular programmed stimulation and incremental frequency stimulation (or concomitant intravenous isoprenaline) failed to induce ventricular tachycardia.
(3) Rapid pacing of the right ventricle for 10 seconds at a time shows changes in the Q-T-U interval and U-wave amplitude caused by sudden deceleration after rapid pacing, which are positively correlated with interval length and pacing frequency.
Diagnosis.
Tachycardia is characterized by tip-twist ventricular tachycardia, with a prolonged Q-T interval, T, U changes, long-short circumference, and R-on-T dyadic ventricular pre-systole inducing a long interval-dependent TDP, with episodes of 3 to 5 seconds, which can be terminated on their own, but are recurrent.
Differential Diagnosis
It is very difficult to differentiate tip-torsion type ventricular tachycardia from other polymorphic ventricular tachycardia, mainly based on its prolonged Q-T interval, U wave, often without severe organic heart disease, with a specific etiology, often recurrent and self-terminating episodes and other characteristics.
1. Differentiate from general ventricular tachycardia or ventricular fibrillation.
General ventricular tachycardia manifests as a series of wide QRS waves with almost fixed morphology, ST segment and T wave can be recognized, and the occurrence will not stop on its own; general ventricular tachycardia can also be induced by RonT ventricular tachycardia, but ventricular tachycardia has a shorter pairing spacing, and in ventricular fibrillation, QRS waves and ST segments cannot be recognized, ventricular rate is greater than 300 beats/minute, extremely irregular, and will not be terminated on its own, and the electric shock resuscitation is effective, and the TDP’s In TDP, the QRS wave and ST-T wave can be recognized, the ventricular rate is mostly around 200 beats/minute, the duration of the attack is short, and the attack will terminate on its own, but it can be repeated, and the effect of electric shock resuscitation is poor.
2. Differentiate from other polymorphic ventricular tachycardia and ventricular fibrillation.
The following two points are helpful for differential diagnosis: (1) the presence of prolonged Q-T interval and U wave, relatively long inter-rhythmic intervals, or typical evoked sequence (long and short circumferences) on the ECG before or just after the onset of ventricular tachycardia is supportive of TDP; (2) the clinical situation at the time of ventricular tachycardia is helpful for the differential diagnosis.
Treatment
1. Remove the triggers
If stop using antiarrhythmic drugs, correct electrolyte disorders, especially timely correction of hypokalemia, and magnesium supplementation, because hypokalemia is not corrected, hypokalemia is also difficult to correct. Some bradyarrhythmias are caused by primary heart diseases, so they and the primary disease should be actively treated.
2. Drug therapy
(1) Isoproterenol is administered intravenously. Isoproterenol can enhance the outward potassium current, accelerate repolarization, shorten the Q-T interval, inhibit early after depolarization, and prevent and control TDP, but it may deteriorate part of ventricular tachycardia into ventricular fibrillation, and should be used with caution, and is more suitable for those who have TDP caused by bradycardia but do not have the condition to do cardiac pacing immediately.
(2) Intravenous potassium supplementation.
(3) Magnesium sulfate can be the drug of choice. The first dose is slowly pushed intravenously, and then intravenously, maintained for 7 to 48 hours, or until the Q-T interval is shortened to <500 milliseconds and then discontinued. There are no adverse effects except flushing. Magnesium sulfate can shorten the relative myocardial response period, prolong the absolute response period, increase the threshold of ventricular fibrillation, and homogenize the repolarization, reduce or eliminate the refractory excitation. It promotes the entry of K into the cell, stabilizes the membrane potential, and corrects the discrete repolarization process, thus preventing and treating the onset of TDP.
(4) Lidocaine can be tried when the above drugs are ineffective, and can be injected intravenously during TDP episodes. The dosage should be sufficient and the time should be long. Its efficacy is variable. It may be ineffective. TDP has been reported in cases of overdose. Lidocaine should not be applied in people with atrioventricular block, sick sinus node syndrome, and slow basal heart rate.
(5) When the above treatments fail, phenytoin sodium IV may be tried. The use of verapamil IV push has been reported to be effective in TDP occurring in the presence of AV block. Antiarrhythmic drugs of class IA, Ic and III are prohibited, and class IB drugs or carbamazepine can be tried.
3. Placement of temporary artificial pacemaker
It is safe and reliable. It should be preferred by those who have the condition. If the condition permits, cardiac pacing can also be performed when the above treatments are ineffective, which can shorten the Q-T interval, eliminate bradycardia, and prevent further aggravation of arrhythmia. Ventricular pacing is preferred to atrial pacing, especially in patients with atrioventricular block. Atrial pacing can also be used in patients without AV block, but it may induce new episodes of ventricular tachycardia if atrial pacing fails to achieve 1:1 conduction. If the patient has high or complete AV block or sick sinus node syndrome, an implantable cardioverter-defibrillator (ICD) should be installed.
4. Electrical cardioversion
Usually, TDP episodes last only a few seconds to tens of seconds and then terminate on their own, and no electrical resuscitation is needed because of the short duration. However, when TDP episodes last for a long time, the ventricular rate is fast, hemodynamics is significantly affected, or the metamorphosis into ventricular fibrillation, synchronized DC cardioversion (50J) should be performed. It is mostly effective in terminating TDP, at least temporarily, and can terminate TDP episodes. Some TDP secondary to high doses of class I A drugs may require repeated electrical reversals to restore rhythm due to an increased threshold for defibrillation, with a success rate of about 65% with a single electrical reversal.