Tachycardia Basics

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Teaching Points:

  • An overview of all forms of tachycardia
  • Important differentiation into narrow/wide and irregular/regular
  • What forms of supraventricular tachycardias are there?
  • All about sinus tachycardia
  • Mechanisms of tachycardia

Tachycardia overview

First, let’s take an overview of all forms of tachycardia.

There are 15 major types, and each is classified according to ECG criteria. Some of these 15 forms of tachycardia can be further subdivided into a group of very similar tachycardias. Atrial flutter, for instance, can be further subdivided into typical and atypical forms. Similarly, ventricular tachycardias have different mechanisms and morphologies.

At the end of this chapter you will have mastered this overview of the 15 major forms of tachycardia.

What is the best approach to sort out the different tachycardias?

QRS width = QRS duration

The most important, and rather general, ECG criterion relates to the width of the QRS complex. A QRS complex is considered narrow if it is no longer than 120 ms (or 0.12 seconds). Using this criterion, we can divide the 15 major forms of tachycardia into roughly two halves: namely, narrow and wide QRS complex tachycardias.

Regularity of QRS complexes

Next, we apply the criterion of regularity. This refers to the distance between two successive ventricular excitations. For this classification, atrial excitation is ignored.

If we combine the two criteria "narrow" or "wide" and "regular" or "irregular", four categories emerge:

Narrow and regular;

Narrow and irregular;

Wide and regular; and

Wide and irregular.

Ventricular fibrillation is a bit out of the ordinary, because here, excitation is so diffuse that it is impossible to divide it into the four categories described above. But we shouldn’t be thinking too much when we see this rhythm: we need to run and get the defibrillator! We’ll look at a few more details on this one later.

Now, let’s go through the four categories systematically.

Narrow complex tachycardias

Here are several facts that you should remember:

As we saw earlier, the normal anatomical and physiological path of excitation begins in the sinus node and passes through the atria to the AV node. In all rhythms with a narrow QRS complex, the excitation is conducted from the AV node via the His-Purkinje system, so the excitation of all tachycardias with a narrow QRS complex proceeds along this path.

Narrow complex tachycardias are usually NOT life-threatening. However, wide-complex tachycardias of ventricular origin can lead very rapidly to potentially life-threatening hemodynamic instability.

We have already mentioned that a narrow QRS complex always reflects excitation via the His-Purkinje system, since this is the only way to synchronously excite the two ventricles in a short time (that is, in less than 120 ms). The origin of a tachycardia with a narrow QRS complex must therefore be upstream of the His-Purkinje system and thus lies within the atria. So if we see a narrow complex tachycardia, it makes sense to include all supraventricular tachycardias in our differential diagnosis.

Let's take another look at our overview:

There are seven major forms of tachycardia in which a narrow QRS complex occurs. In six of these, the QRS complex is narrow and regular, and in one form, namely atrial fibrillation, the QRS complex is narrow and irregular.

All narrow complex tachycardias have a supraventricular origin.

However, not all supraventricular tachycardias have a narrow QRS complex. If this were the case, one could simply stop at the division into narrow and wide, and classify according to etiology only.

Now, why can a supraventricular tachycardia have a wide QRS complex? The answer is simple:

A bundle branch block, or a so-called aberrancy. You will recall from the chapter on bundle branch block that a total bundle branch block is defined by a QRS width of 120 ms or more.

We have already mentioned that, for the most part, narrow complex tachycardias are not life-threatening, whereas wide complex tachycardias with ventricular origin can lead very rapidly to hemodynamic instability.

In detail, this implies that supraventricular tachycardias, which employ the His-Purkinje system, do not degenerate into ventricular fibrillation: They only become hemodynamically relevant if they are very fast or if the heart is already severely impaired; for example, if ventricular function is significantly impaired or if concomitant valve disease, such as aortic stenosis, is present.

To ensure patient safety, the following rule applies in clinical practice:

All wide QRS complex tachycardias are of ventricular origin until proven otherwise.

It is now up to us to prove the opposite. Caution: No matter how prompt and correct we are in obtaining this proof, any tachycardia must be terminated as soon as possible if your patient is hemodynamically unstable, irrespective of whether the QRS complex is wide or narrow.

Sinus tachycardia

Before we look at narrow complex tachycardias, let’s first consider the most simple narrow complex tachycardia: sinus tachycardia. This is a disorder that can be diagnosed instantly through a quick visual inspection of the ECG tracing.

Sinus tachycardia is not really considered an arrhythmia. It is the physiological response of the body under stress. This finding is so frequent that it is precisely for this reason that the correct ECG criteria of a sinus tachycardia are of importance in your daily clinical work.

Three simple criteria are used to confirm sinus tachycardia:

1. The ventricular rate must be tachycardic, that is above 100 bpm. Otherwise, it would not be a tachycardia, but a normal sinus rhythm.

2. There must be exactly one P wave before each QRS-complex.

3. The heart rate must be variable and influenced by external factors, for example, by exertion.

That sounds simple enough. But is it really? Even if at first glance an ECG suggests a sinus tachycardia, there may be other rhythm disturbances concealed behind it. The best way to distinguish between these rhythm disturbances will be explained in the following chapters.

In addition, sinus tachycardia is usually the expression of the activation of the sympathetic—or rather the suppression of the parasympathetic—nervous system. In routine clinical practice, we should therefore ask:

Is there any other trigger for the tachycardia, besides acute physical exertion, and do I have to fix it? Typical examples include all forms of shock; pulmonary embolism; hemorrhage; respiratory insufficiency; metabolic acidosis; illicit drug use, such as for example amphetamines; anxiety; and many more.

You can see there is a variety of reasons for a sinus tachycardia, which is often referred to as a "demand tachycardia". The therapy will always depend on the underlying cause.

Mechanisms of tachycardia

To improve your understanding of the supraventricular tachycardias presented in the following section, let’s consider the common mechanisms that underlie tachy-arrhythmias:

1.Macro Reentry

This refers to a situation in which depolarization runs along a circuit through anatomical structures that are electrically insulated. These abnormal circuits may be congenital or acquired. For this to occur, the anatomical structures must contain excitable cells and the circuit must last long enough. The initially excited cells must have become repolarized by the time the wave of depolarization reaches the beginning of the circuit again. Usually, slow conduction structures are responsible for Macro reentry circuits.

Typically, these circuits are located around the tricuspid valve, within the AV node, or around myocardial scars. The detailed course of the circuits is explained in more detail in the discussion of individual arrhythmias. Depending on the course of the circulatory excitation, it may involve the atria only, the ventricles only, or both the atria and the ventricles. In the 12-lead ECG, we see regular electrical potentials, whose precise morphology depends, of course, on the circuit’s pathway.

2. Micro-Reentry

Here, the mechanism is identical to that of macro-reentry, except that no particular pathway can be detected. Myocardial scars also play an important role in micro-reentry.

3. Automatism

Individual myocardial cells can spontaneously depolarize. This is the principle of excitation in the sinus node. If cells other than the sinus node show spontaneous activity, this is called an automatism. This leads to premature atrial and ventricular beats. If one of these cells fires at a high rate, a tachycardia is generated.

4. Atrial fibrillation and ventricular fibrillation

These are special forms of tachycardia. Both involve the completely chaotic spread of excitability in either the atria or the ventricles.

There is one further reason for a tachycardia: if the heart rate specified by the electrocardiograph seems too high, you should measure it manually. This may sound trivial, but in reality, a false machine reading happens more often than you might think. In most cases, the heart rate on the machine is twice as high as it really is because the machine has counted T waves as R waves.

In the following chapters, we will look at the other supraventricular tachycardias.