Ectopic Foci and Their Morphologies

The basic beat was discussed in depth in Chapter 4, Vectors and the Basic Beat. This section deals with variations in the morphology of the complex based on where the complex originated in the heart. The exact location or focus that acts as the main pacemaker for a complex dictates the appearance of the complex. This is due to many factors, and we will address them individually in the pages to come. For now, take a look at Figure 6-10 to get an overall impression of the location of a particular focus and its associated morphology characteristics.

Figure 6-10 Ectopic foci and the respective morphology of the complexes.

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There are many factors that affect the morphology of the complexes on an ECG. The main ones include the actual pacemaker site and the route that the impulse has to take to cause depolarization of the entire heart. These topics will be discussed in much greater detail as needed in subsequent sections of the book, but for now we will have an introductory discussion.

Let’s start off by looking at the ectopic atrial sites. Since we are talking about atrial sites, the changes will be seen in the P waves and that is where we will begin. If you remember from Chapter 4, Vectors and the Basic Beat, a positive vector heading toward an electrode will be interpreted on the ECG as a positive wave (Figure 6-11). A positive vector headed away from an electrode will be interpreted as a negative wave on the ECG (Figure 6-12). Vectors dictate morphology; directions of the depolarization waves on the heart dictate vector direction and vector size.

Figure 6-11 In this example, the P-wave vector is headed inferiorly, backward, and to the left. Leads I and II see a positive vector headed toward them, and this is represented electrocardiographically as a positive P wave in those leads.

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Figure 6-12 In this example, the P-wave vector is headed superiorly, backward, and to the right. Leads I and II see a positive vector headed away from them, and this is represented electrocardiographically as a negative P wave in those leads.

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When you have an ectopic focus acting as the pacemaker for a complex, the angle and direction of the main atrial vector (also known as the P-wave axis) will be different from one that originated in the sinus node. For simplicity, Figure 6-12 shows a vector that originated in the inferior aspect of the left atria and travels superiorly, backward, and to the right. This vector is seen by the electrodes for leads II, III, and aVF as heading away from them, and so will give rise to a completely negative or inverted P wave. As you can imagine, there are quite a large number of possible ectopic pacemakers, and therefore, quite a large number of possible P-wave morphologies. The important thing clinically, is that ectopic P waves are all different morphologically from the sinus P waves. Picking up on these differences is key to making the correct diagnosis.

Now, let’s turn our attention to the atrioventricular (AV) node. When the AV node functions as the primary pacemaker for a complex, one of two things will happen: (1) There will be no P waves or (2) the P wave will always be inverted in leads II, III, and aVF.

In Chapter 1, Anatomy and Basic Physiology, we saw that the AV node is the only connection between the atria and the ventricles under normal circumstances. If it were not for the AV node, the atria and ventricles would actually function completely oblivious to each other. The AV node is, essentially, the gatekeeper for the heart, allowing communication to proceed back and forth. We saw that the gate can either be opened, allowing impulses to travel back and forth between the atria and the ventricles, or it can be closed, blocking impulse transmission between the two.

Now, suppose you had a large empty container meant to hold water with two sides, compartments A and V (Figure 6-13). There is a wall in the middle acting as a dam to prevent water from traveling back and forth between the two sides. The dam has a lock in the middle with two gates that could be opened to allow movement of water back and forth between the compartments. Suppose you filled the lock, right between two gates, with water (Figure 6-14). What would happen if you opened the gate on the right? The water would flow into compartment V. Compartment A would be dry and unaware of the flooding occurring in compartment V.

Figure 6-13 A large container with a central lock and two gates in the middle. The gates and the lock allow controlled communication between the two sides of the containers.

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Figure 6-14 If the lock in the middle of the container were filled with water and the right gate opened, the water would flow into compartment V and spread evenly throughout that side of the container.

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The same thing can happen when the AV node acts as the primary pacemaker. The junctional focus fires, causing an impulse to start to develop. This is equivalent to filling the lock with water. In our analogy, the next step would be to open the right side of the gate and allow the water to fill compartment V (Figure 6-15). In the heart, the impulse that originated in the junctional focus travels down the electrical conduction pathway, causing a normal depolarization of the ventricles (Figure 6-16). This is represented on the ECG as a normal-looking QRS complex with no P waves. There are no P waves because the AV node did not allow the impulse to travel retrogradely into the atria. To put it another way, the left side of the gate was not opened.

Figure 6-15 The right side of the gate was opened, releasing the contents and filling compartment V.

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Figure 6-16 The impulse that originated in a junctional focus caused normal conduction down the electrical conduction system. The ventricles depolarized normally, forming a QRS complex with a normal morphology.

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This is what occurs if the AV node does not allow the impulse generated in a junctional focus from traveling retrogradely or backward into the atria. This is one possibility. Now let’s turn our attention to the other possibility.

Suppose that both gates on the lock were opened up simultaneously. What would happen to the water in the lock? It would flow into both compartments at the same time (Figure 6-17). This is exactly what happens when a junctional focus fires as the pacemaker of the complex. In this case, the P wave and the QRS complex would both be formed at exactly the same time, leading to a buried P wave (Figure 6-18). The morphology of the QRS complex may be slightly altered or it may appear normal.

Figure 6-17 Suppose both gates on the lock opened up at the same time. The water would flow into both compartments simultaneously. In the AV node, this leads to the P wave occurring early (causing a short PR interval) or at the same time as the QRS complex (causing the P wave to be buried in the QRS complex).

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Figure 6-18 If a junctional focus acts as a primary pacemaker for a complex, the PR interval is shorter than expected or the P wave is buried in the QRS complex. The P-wave morphology would always be inverted in leads II, III, and aVF because of the direction of the vector (see yellow vector) caused by the retrograde atrial conduction of the junctional complex.

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If the junctional focus were closer to the atrial side of the AV node, the retrograde conduction to the atria would occur faster than ventricular depolarization and the P wave would come sooner in the cycle. This morphologically causes a shortened PR interval.

Ectopic Foci in the Ventricles

We have seen how the morphologic changes of the complexes are caused when an ectopic focus in the atria and AV node act as the primary pacemaker. Now, we turn our attention to what happens when the ventricles act as the ectopic focus.

The first thing to notice about any ventricular ectopic focus is that it will lead to very broad, bizarre-looking QRS complexes (Figure 6-19). In addition, the site of the ventricular focus will alter the morphology in its own way. Both of these changes can be understood more easily if you keep in mind that ECG morphology is dictated by vectors. So, you already have the knowledge base to figure out why this occurs. Let’s see how it happens.

Figure 6-19 The firing of a ventricular ectopic focus leads to the formation of wide, bizarre-looking QRS complexes. The Figure shows various types of possible QRS morphologies, but the actual appearance of a QRS cannot be predicted completely based on the location of the ectopic focus. In addition, the morphology will change based on the lead used to view the complexes.

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Use your imagination, and the information you have learned so far in this book, to try to figure out the process. How do the ventricles normally depolarize? The impulse comes down the electrical conduction pathway and spreads through the His bundles, the left and right bundle branches, and finally reaches the Purkinje system. The Purkinje system, in turn, stimulates the nearest myofibrils. From that point on, one myofibril stimulates an adjoining myofibril and the rest of the process of ventricular depolarization occurs via direct cell-to-cell stimulation. The organized sequential stimulation of the first set of myofibrils at the same time throughout both the left and right ventricles greatly shortens the process of ventricular depolarization, leading to a nice, normal-looking QRS complex.

Now, what happens when an ectopic focus acts as a primary pacemaker? Is the electrical conduction system stimulated simultaneously, providing a synchronized depolarization wave to occur in both ventricles? The answer is no. When an ectopic ventricular focus fires, the only cells that become stimulated by the depolarization are the ones in direct contact with the ectopic focus. When they, in turn, fire, they only stimulate their surrounding myofibrils, and so forth. This is a process of direct cell-to-cell stimulation that is very time consuming and does not lead to synchronized mechanical contraction. In Figure 6-20, the cell-to-cell depolarization wave is represented by the concentric waves moving outward from the ectopic focus.

Figure 6-20 An irritable focus, represented by the red star, acts as a pacemaker and causes an impulse to occur. This gives rise to a depolarization wave that radiates outward by direct cell-to-cell transmission throughout both of the ventricles. Note the color-coded sections of the depolarization wave and the complex.

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How would this direct cell-to-cell transmission of the ventricular depolarization wave look morphologically on an ECG? It depends on the vector that it forms, but it would definitely be wide because of the slow nature of the conduction. Remember, what leads to a nice, tight QRS complex is the synchronized conduction of the depolarization wave. An ectopic focus leads to asynchronous depolarization, which is very slow. Time on an ECG is demonstrated in the horizontal direction, hence the wide presentation on the complexes.

Now on to why the complexes are bizarre in appearance. Under normal circumstances, the synchronous depolarization of both ventricles leads to the formation of three almost simultaneous vectors (Figure 6-21). These vectors give rise to distinct morphologic ECG representations that form the QRS complex: the Q wave, the R wave, and the S wave. With the firing of a ventricular pacemaker, do you have the formation of the same three distinct vectors, or do you have the formation of a haphazard series of vectors? The answer is a haphazard series of vectors. How these vectors align temporally will decide the final morphology of the QRS complex.

Figure 6-21 The synchronous depolarization of the ventricles by the electrical conduction system gives rise to three main vectors. The first one, represented by the red vector, will give rise to the Q wave. The second vector, represented by the yellow vector, will give rise to the R wave. The third vector, the blue vector, gives rise to the S wave. The three vectors are represented on the QRS complexes (as they appear in their particular leads) by their respective colors.

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