Regardless of the etiology and ECG, ventricular tachycardia is always a potentially life-threatening arrhythmia that requires immediate attention. The heart rate is usually very high (100-250 beats per minute), and the minute volume (ejection) of blood is affected (i.e., reduced) in almost all cases.
This type of tachycardia causes a huge load on the ventricular myocardium at the same time, since the cause of arrhythmia already affects cellular function. This leads to electrical instability, which explains why it can progress to ventricular fibrillation.
If untreated, it leads to asystole and cardiac arrest. All health care providers, regardless of profession, should be able to diagnose paroxysmal ventricular tachycardia on an ECG. Description and how to do it - next.
Causes
Patients with paroxysm of ventricular tachycardia on an ECG almost always have a significant heart ailment. The most common causes are:
- coronary heart disease (acute coronary syndromes);
- heart failure;
- cardiomyopathy (expanded, hypertrophic or obstructive);
- valvular disease.
Less common causes are:
- arrhythmogenic cardiomyopathy / dysplasia of the right ventricle (ARVK / ARVD);
- Brugada syndrome;
- prolonged QT syndrome;
- sarcoidosis;
- Prinzmetall angina angina (coronary vasospasm);
- electrolyte disturbances;
- congenital heart defects;
- induced by catecholamine;
- ventricular tachycardia.
The vast majority of patients with ventricular tachycardia have:
- coronary artery disease (coronary heart disease);
- heart failure;
- cardiomyopathy;
- valvular heart disease.
In these populations, one of the strongest predictors of sudden cardiac death is left ventricular function. Individuals with reduced left ventricular function (for example, defined as an ejection fraction <40%) are at high risk for sudden cardiac arrest.
Idiopathic Ventricular Tachycardia (IVT)
This pathology can be classified as idiopathic, if no cause of its occurrence can be identified. This diagnosis has a more favorable prognosis compared to other forms. So he looks on an ECG.
Ventricular Tachycardia Mechanisms
This pathology (VT) can occur due to increased / abnormal automaticity, re-entry or operation. All types of myocardial cells may be involved in initiating and maintaining this arrhythmia. As mentioned above, VT causes a hemodynamic compromise. The fast work of the ventricles, which may be accompanied by a violation of their functions, does not allow them to adequately fill up, which leads to a decrease in stroke volume and a decrease in cardiac output.
It is worth examining in more detail the signs of ventricular tachycardia on an ECG (paroxysmal). More on that later.
Ventricular tachycardia in acute coronary syndromes (myocardial infarction)
Acute coronary syndromes are divided into:
- unstable angina pectoris (UA);
- ST myocardial infarction (STEMI);
- myocardial infarction without ST (NSTEMI).
Under these conditions, the risk of VT is very high. In addition, it is very time-dependent, it is the highest in the phase of hypertension (first minutes to several hours after the onset of symptoms).
The vast majority of people who die in the acute phase of myocardial infarction actually die from ventricular tachyarrhythmias. Death due to pumpdown failure is less common. Since the risk is highest in the first minutes to several hours, most deaths occur outside the hospital. The risk of BT (and, consequently, ventricular fibrillation) gradually decreases over time. In addition to timing, the main determining factor for VT is the degree of ischemia / heart attack.
Features and criteria of an ECG of ventricular tachycardia
≥3 consecutive ventricular rhythms at a speed of 100-250 beats per minute (in most cases> 120 beats per minute).
At a speed of 100 to 120 beats per minute, it is called slow ventricular tachycardia.
At a speed of> 250 beats per minute, ventricular flutter.
Wide QRS complexes (QRS duration ≥0.12 s).
Types
An ECG of ventricular tachycardia may indicate a subclassification of the disease. The data below can be perceived as advanced, but it is not necessary that all clinicians can classify the disease according to the cardiogram: just recognize its presence.
Stable and unstable ventricular tachycardia
Running ventricular tachycardia on an ECG has two directions. Durations <30 seconds are classified as unstable. Sustainable has a duration of> 30 seconds.
Monomorphic
In monomorphic ventricular tachycardia, all QRS complexes have the same morphology (slight differences are allowed). This indicates that the impulses occur at the same ectopic focus. In structural heart disease (coronary heart disease, heart failure, cardiomyopathy, valvular disease, etc.) Usually caused by re-entry.
Purkinje fibers in the interventricular septum, apparently, play an important role in the development of this pathology in patients with coronary heart disease. These fibers are strongly arrhythmogenic in conditions of myocardial ischemia, especially repeated. Since any impulse arising in the interventricular septum will enter the Purkinje network (to some extent), QRS complexes tend to be shorter than arrhythmias originating from the walls of the free ventricles. The duration of QRS is usually 120 to 145 ms in ventricular tachycardia occurring in the septum.
The focal type is the idiopathic form of VT. This is caused by repeated entry into the bundles of the left branch (i.e., in Purkinje fibers). Focal ventricular tachycardia occurs in people under the age of 50 years and mainly in men. QRS complexes display a morphology similar to the block of branches of the right bundle, and there is a deviation of the left axis.
Ventricular tachycardia is a monomorphic VT that occurs in the outflow of the right ventricular tract. Arrhythmia is mostly idiopathic, but some patients may have ARVC (arrhythmogenic right ventricular cardiomyopathy). Since pulses arise in the right ventricle, the QRS complexes have the form of beam branches, and the electrical axis is about 90 °.
Polymorphic
Ventricular tachycardia with varying QRS morphology or the electrical axis is classified as polymorphic. ECG ventricular tachycardia type pirouette has the following meanings:
- The rhythm may be irregular. Polymorphic is usually very fast (100-320 beats per minute) and unstable. There are several types of polymorphic ventricular tachycardia. The most common cause is myocardial ischemia. The second most common cause is a long QTc interval (Long QT syndrome).
- Familial catecholaminergic polymorphic ventricular tachycardia (CPVT) is hereditary, in which emotional or physical stress causes arrhythmia, which can lead to blood circulation and cardiac arrest. This type can be bidirectional. The diagnosis is established using a stress test, because sympathetic activity causes tachycardia.
- Brugada syndrome causes polymorphic BT (mainly during sleep or fever).
Early repolarization and hypertrophic obstructive cardiomyopathy also lead to polymorphic VT.
ECG bi-directional ventricular tachycardia, the photo of which is attached, means that the QRS morphology alternates from one ebat to another. In most cases, it is repeated between two variants of the QRS complex. Observed in familial CPVT, excess digoxin, and prolonged QT syndrome.
With coronary heart disease
Coronary artery disease (coronary heart disease) is by far the most common cause of ventricular tachycardia, and the mechanism is mainly a relapse.
As mentioned earlier in this chapter, re-entry occurs when the central unit is in front of the depolarizing pulse, and the cells surrounding it have different conductivity. In coronary heart disease, the central block is usually the ischemic / necrotic myocardium (which does not conduct any impulses), while the surrounding cells have dysfunctional conductivity due to ischemia. Ventricular tachycardia because of it represents a high risk of degeneration into ventricular fibrillation and cardiac arrest.
Therefore, ventricular tachycardia in coronary artery disease is mainly monomorphic. It can be polymorphic if there are several ectopic foci or the impulse from one focus spreads in different ways. But if ventricular tachycardia without a pulse on the ECG, then you should resort to resuscitation.
Search for ectopic foci causing ventricular tachycardia
The ECG provides valuable information on the location of ectopic foci causing tachycardia. This is done by classifying ventricular tachycardia in the broad sense as “the appearance of a bundle branch” or “the appearance of a branch of a right bundle”.
Ventricular tachycardia with ECG forms resembling the left branching block of the bundle (the dominant S-wave in V1) occurs in the right ventricle. The opposite is also the fact that ventricular tachycardia, resembling a block of branches of the right bundle (the dominant R-wave in V1), occurs in the left ventricle. This can be useful when trying to decipher what may be causing the pathology.
Distinctive
Sometimes supraventricular tachycardia (which mainly have normal QRS complexes, i.e., QRS duration <0.12 seconds), can exhibit wide QRS complexes. This may be due to concomitant block, aberration, hyperkalemia, pre-excitation or side effect of drugs (tricyclic antidepressants, class I antiarrhythmic drugs).
It is important to be able to differentiate supraventricular tachycardia with wide QRS from VT, and the reason for this is simple: VT is potentially life-threatening, while supraventricular arrhythmias are not. Consequently, the wide QRS complexes do not guarantee that the rhythm is ventricular in origin.
Fortunately, there are several characteristics that separate ventricular tachycardia from supraventricular (SVT). They can be used separately or in algorithms (which are easy to use) to determine if tachycardia is with wide QRS or SVT complexes.
Before dwelling on these characteristics and the algorithm, it should be noted that 90% of all common tachycardia is ventricular! If the patient suffers from any of the above conditions as risk factors for ventricular tachycardia, one should be very inclined to assume that it is she.
The characteristics of ventricular tachycardia are currently being discussed.
Atrioventricular (AB) dissociation
AV dissociation means that the atria and ventricles function independently of each other. On the ECG, this manifests itself as P-waves that are not related to QRS complexes (PP intervals differ from RR intervals, PR intervals change and there is no connection between P and QRS).
Note that it is often difficult to detect P-waves during VT (an esophagus ECG can be very helpful). If AV dissociation can be verified, VT is likely to cause arrhythmias. However, sometimes ventricular impulses can be carried out retrograde through the His-node and the AV-node in the atrium and depolarize the atria synchronously with the ventricles; in this way, VT can actually display synchronized P-waves.
Initiation of tachyarrhythmia
If the onset of tachycardia is recorded, it is important to evaluate the initial rhythms. If the RR intervals were initially irregular, this indicates ventricular tachycardia. This is called a deforming phenomenon. Supraventricular tachycardia does not show warm-up (with the exception of atrial).
Electric axis
An electrical axis between -90 ° and -180 ° indicates ventricular tachycardia (although antidromic AVRT is a differential diagnosis). If the electric axis during arrhythmia differs> 40 ° from the sinus axis, this also indicates this pathology.
If tachyarrhythmia has the correct beam branch diagram, but the electrical axis is more negative than -30 °, this indicates ventricular tachycardia.
If tachyarrhythmia has the structure of the block of branches of the left bundle, but the electric axis is more positive than 90 °, this also speaks of it. In general, a deviation in the left axis indicates this pathology.
QRS Duration
QRS duration> 0.14 s indicates ventricular tachycardia, as does QRS> 0.16 s. Please note that ventricular tachycardia that occurs in the interventricular septum may have a relatively narrow QRS complex (0.120-0.145 s). Anti-dermal AVRT may also have> 0.16 s. Class I antiarrhythmic drugs, tricyclic antidepressants, and hyperkalemia can also cause very wide QRS complexes.
Harmonization in V1-V6
This means that all QRS complexes from lead V1 lead the V6 head in one direction; they are all either positive or negative. If any lead displays two-phase QRS complexes (for example, qR complex or RS complex), then there can be no coordination.
Negative by analogy (all QRS complexes are -) strongly indicate ventricular tachycardia. Positive coordination (all QRS complexes +) is mainly due to it, but can be caused by anti-dermal AVRT.
It is not recommended to administer "Adenosine" when ventricular tachycardia is suspected, because it can accelerate the frequency and worsen arrhythmia. Sometimes it is still used when it is suspected that arrhythmia is actually an SVT with wide QRS complexes. But if the drug has no effect or speeds up the heartbeat, it is most likely ventricular tachycardia.
This is the most used algorithm.
Brugada syndrome
If there is no RS complex in any chest (V1-V6), a diagnosis of ventricular tachycardia can be made. Otherwise, proceed to the following criteria.
Estimate the RS interval (the interval from the beginning of the R-wave to the nadir of the S-wave). If any RS interval is> 100 ms and the R-wave is wider than the S-wave, a ventricular tachycardia can be diagnosed. Otherwise, proceed to the following criteria.
With AV dissociation, ventricular tachycardia can be diagnosed.
Assess the QRS morphology in V1, V2, V5, and V6 (see below). If it is compatible with ventricular tachycardia, then the diagnosis is clear.
If the criteria are not met, supraventricular tachycardia can be diagnosed.
Long term treatment
Patients with an increased risk of sudden cardiac arrest (decreased left ventricular function, previous myocardial infarction, structural heart disease) should be considered in the ICD, which provides effective protection.
Depending on the type of tachycardia, either antiarrhythmic drugs or antarrhythmic drugs are prescribed. The first ones are those shown in the photo above.
Among the latter, the most effective ones are shown in the following image.
As can be seen from the table, Amiodarone is in the first place and, apparently, is the most effective drug for the prevention of new episodes of ventricular tachycardia.