Ventricular Tachycardia

In the previous chapter, you learned that each narrow complex tachycardia passes through the physiological conduction system and thus must have a supraventricular origin. In the case of wide QRS complex tachycardias, determination of the origin is not so easy.

In everyday life, the patient's position may help you. If he is still standing, it is probably a supraventricular tachycardia. If he is unable to stand up or is even unconscious, it instantly makes a ventricular tachycardia much more likely. Since a ventricular tachycardia, or VT for short, is clearly more dangerous than a supraventricular tachycardia or SVT for short, a wide complex tachycardia is treated as VT until proven otherwise. Therefore, in this chapter, we will first explain the important aspects of VT.

An explanation of how to distinguish a VT from SVT is provided in a later chapter.

Before we turn to the identification of the VT in the ECG, let’s consider a few fundamental characteristics of ventricular tachycardia:

A VT is a tachycardia that originates from the ventricle. Depending on heart rate and duration, it can cause symptoms such as lightheadedness, palpitations, syncope, and even cardiac arrest. We then speak of a hemodynamically relevant VT.

Every VT can degenerate into ventricular fibrillation at any time. Thus, even in a patient with a well-tolerated slow VT who tells you he is fine, be prepared for instant resuscitation since the situation can get out of control within seconds.

The causes of VT are manifold. In general, the worse the left ventricular function, the higher the risk of VT.

In most cases, the acute mechanisms are an ischemia-induced electrical instability of the myocardial cells OR micro- and macro-reentry tachycardias secondary to structural heart disease. Frequently, the excitations circulate in or around scar tissue, which has resulted from a previous myocardial infarction. However, micro-reentry tachycardias may also arise from dilated or hypertrophic cardiomyopathies, due to the occurrence of structural changes at the microscopic level.

Certain gene defects, especially those affecting ion channels, can also cause ventricular tachycardias. The most common hereditary rhythm disorders are Long QT syndrome, Brugada's syndrome, and arrhythmogenic right ventricular cardiomyopathy. A relevant extension of the QT time may also be caused by medication or electrolyte changes.

Ventricular tachycardias can be classified in different ways. Let’s start with two easy ones, which are of great clinical importance:

First, we can differentiate "non-sustained VT" or "nsVT" from sustained VT’s. The cut-off for VT duration has been set arbitrarily at 30 seconds. Sometimes, patients have numerous premature ventricular beats.

Differentiating these from an nsVT can be confusing. By definition, when you find four premature ventricular beats or more in a row with at least 100 beats per minute, this is called an nsVT.

Secondly, it is important to know whether a VT is hemodynamically compromising or not, that is, whether the VT leads to a significant drop in blood pressure. However, remember that while a patient with VT may be hemodynamically stable at presentation, their condition may deteriorate significantly thereafter.

The third classification applies exclusively to ECG criteria. A distinction is made between so-called monomorphic and polymorphic VT. Monomorphic means that the QRS complexes within a running VT are very similar and are spaced at regular intervals. In the case of polymorphic VT, the QRS complexes differ in their morphology and thus also in terms of their distance from one another and their duration. This classification has both prognostic and therapeutic significance. In principle, polymorphic VT is more dangerous, because it degenerates more quickly to ventricular fibrillation. However, the initial heart rate is, of course, also crucial in terms of risk and prognosis. We will go into this in more detail later.

First, let's look at the typical ECG characteristics of a VT:

The heart rate is usually between 150 to 250 beats per minute. In rare cases, the rate is slower, but this is usually due to existing antiarrhythmic therapy such as ajmaline or amiodarone.

The duration of ventricular excitation, or the length of the QRS complex, is usually longer than 140 ms due to the lack of any connection to the conduction system. Often, we find a QRS width of 160 ms or even much more.

As usual, the wideest QRS complex in the 12-lead ECG determines the true QRS duration, even if it is narrower in all other leads.

The tips of the R wave and the T wave often have a different vector; one is positive and the other negative, or the other way around. We call this an R-T discordance.

The main vector is often found in “no-man’s-land"; that is, the electric heart axis is not definable at all.

The most common form of ventricular tachycardia is monomorphic VT. Here, the heart rate is usually around 150-250 beats per minute. A patient with monomorphic VT and a heart rate of above 250 per minute is often hemodynamically stable, and can be diagnosed as having “ventricular flutter”. A patient with a slower monomorphic VT can be stable for many hours without hemodynamic decompensation. However, the heart rate does not guarantee stability: each VT can accelerate to ventricular flutter at any time, or degenerate into ventricular fibrillation.

Monomorphic ventricular tachycardias include idiopathic right ventricular outflow tract tachycardia. In the ECG, a relatively narrow QRS complex and a left bundle branch block configuration are observed. The heart rate is usually below 160 per minute. The prognosis is significantly better than in patients with a VT that develops secondary to structural heart disease.

Polymorphic ventricular tachycardias occur in different constellations. In the case of polymorphic VT without QT prolongation, severe structural heart diseases or acute ischemia due to myocardial infarction are often responsible. No uniform morphology is found when comparing the different QRS complexes. The higher the heart rate, the closer we get to ventricular fibrillation.

The polymorphic VTs also include a special form, which occurs as part of a long QT syndrome. If the QT time is too long, a premature ventricular beat may fall into the vulnerable phase of the partially refractory myocardium. This results in the so-called "torsade de-pointes tachycardia". In this example, we see the typical wavelike increase and decrease of the amplitude with the tips of each QRS complex pointing first upwards and then downwards.

The prognosis is poorer, since degeneration into ventricular fibrillation occurs more frequently and more rapidly than in the case of monomorphic ventricular tachycardias.

Ventricular flutter is a rapid, regular form of ventricular tachycardia.

Depending on which academic source you consult, the diagnosis requires a heart rate of between 200 and 300 bpm or more. Because of these high rates, ventricular flutter often leads to cardiac arrest, and rapidly degenerates into ventricular fibrillation.

Even as ECG enthusiasts, we should not waste time trying to differentiate ventricular flutter from other life threatening arrhythmias. Instead, we should be running to get the defibrillator.

Ventricular fibrillation is the term used to describe chaotic excitation within the ventricles. It always leads to cardiac arrest, and resuscitation must therefore be started immediately.

In the ECG, we no longer see QRS complexes or other regular excitations. As a rule, the longer it persists, the lower the amplitude.

Ventricular fibrillation can be diagnosed instantly through a glance at the ECG tracing. Early defibrillation is critical to the prognosis of the patient.