Bradycardia Part 1

To detect bradycardia on the ECG, you must first be familiar with three basic principles.

It helps to...

1. know the anatomy and physiology of the heart’s conductive system.
2. understand the relationship between the waves and intervals that are seen on the ECG tracing and the underlying processes within the conductive system.
3. have a clue how to determine the heart rate, both in the atrium and in the ventricles.

These three points have been covered in previous chapters. If you are still unsure about any of them, go back and review them before continuing here.

The cycle of cardiac excitation begins in the sinus node. The sinus node is a collection of specialized myocardial cells which spontaneously depolarize. The excitation spreads in the heart from cell to cell. The sinus node excites the adjacent atrial myocardium. First, both atria are depolarized. The excitation then reaches the AV node, which forms the electrical connection between the atria and the chambers. The AV node delays the electrical excitation, then passes it on over the His bundle to the Tawara branches. These high-speed lines lead into both chambers. The chamber myocardium has the property that the most recently depolarized cells repolarize the earliest.

During chamber excitation, the atrium is already repolarized and ready to receive the next excitation from the sinus node. The cycle is complete.

The clinical symptoms are caused by hemodynamically relevant bradycardias. Patients typically suffer from dizziness, weakness, and syncopes, sometimes with vagal symptoms or angina pectoris Chest pain. Bradycardia can result from damage to either the sinus node or the AV node.

Sinus node dysfunction may be intermittent or permanent.

When we talk about disorders of the sinus node, it is important to know the following terms that are all expressed by a pathological sinus node: sinus node syndrome, sick sinus syndrome, sinus node dysfunction, sinus node disease, sinu-atrial disease, and bradycardia-tachycardia syndrome.

A functional disorder of the sinus node is a disease of the excitation and conductive system. This disease often manifests itself not only in the sinus node, but also in the other parts of the conduction system such as the AV node or the Tawara branches. This explains the frequent coincidence of a sinus node disease with an AV block or bundle branch block.

Like the AV node, the sinus node can also be damaged for various reasons, resulting in noticeable consequences for the excitation and the contraction process.

In contrast to the AV block, depolarization of the sinus node is not visible on the surface ECG. This makes a diagnosis of sinus node dysfunction rather tricky.

The only two indicators of sinus node dysfunction are the absence of P waves or the presence of variable P-to-P intervals.

The P wave represents the excitation of the atria in the ECG. As we learned earlier, the prerequisites for the formation of a P wave are depolarization of the sinus node and the successful conduction of this excitation into the atrial myocardium. If the P wave is absent, there is either a disturbance of the depolarization of the sinus node, or a problem with the transfer of the depolarization from the sinus node to the atrial myocardial cells.

In the first case, that is, if there is a failure in depolarization, we have what is known as a sinus node arrest. However, the term sinus node arrest is only used if none of the heart’s pacemaker centers generate any excitation and thus a pause, or asystole, prevails.

When conduction from the sinus node to the atrial myocardium is delayed or impaired, we call this sinus node block or sinuatrial block. As with AV block, sinuatrial block is divided into three degrees. And as with AV block, second degree SA block is divided into two sub-categories.

These degrees are pathophysiologically identical to those of AV block, however, they are displayed quite differently in the ECG.

The sinuatrial block, or SA block, refers to a delay in the spread of excitation from the sinus node to the atrial myocardium. Sinuatrial block degree 1 is not visible in the surface ECG and is generally irrelevant in everyday life.

Second degree sinuatrial block type 1 is also known as Mobitz type 1. It refers to any delay in the spread of excitation from the sinus node to the atrial myocardium that increases with each depolarization of the sinus node. At the end of a cycle, sinuatrial transition is completely lost.

Because the firing of the sinoatrial node is not visible on the ECG tracing, the delay between excitation of the sinus node and the atrial myocardium cannot be seen on the surface ECG. A marker that is visible in the surface ECG, such as the previous P wave in the AV block is missing.

Paradoxically, the P-P distance shortens with each excitation. This is because although the delay between sinus node and atrial myocardium increases with each sinus depolarization, the degree of increase becomes less with every beat.

Unfortunately, this is usually not recognizable in the ECG.

Second degree SA block type 2 is also known as  Mobitz type 2, and usually presents as sinus bradycardia or sinus arrhythmia.

It is characterized as an intermittend complete impairment of conduction from the sinoatrial node to the atrial myocardium. For example, only every 2nd, 3rd, or n-th firing of the sinoatrial node spreads to the atrial myocardium. The resulting rhythm is half, a third, or a fifth of the actual sinoatrial heart rate. Since the body usually reacts to bradycardia-induced hypotension and reduced tissue perfusion with an increase in the sinus node rate, it is impossible to determinethe exact rate of conduction on the surface ECG. If the heart rate falls below the spontaneous depolarization rate of the secondary pacemaker centers, a periodic replacement rhythm typically arises.

In the 3rd degree sinuatrial block, the P waves are completely absent. On the surface ECG, 3rd degree sinuatrial block cannot be distinguished from a sinus node arrest. In a patient with an otherwise healthy heart, an AV-junctional replacement rhythm with a narrow QRS complex is usually seen. If the AV node is also diseased and a periodic rhythm is absent, a tertiary pacemaker center usually becomes active, with the generation of a ventricular replacement rhythm. We will learn more about this in the chapter on AV block.

Pre-automatic pauses arise after the conversion of atrial fibrillation into a sinus rhythm. The phrase pre-automatic pause refers to a situation in which an asystole occurs before the onset of the "automatic" excitation. The so-called "automate" is, of course, the sinus node. Therefore, pre-automatic pauses are another form of sinus node dysfunction.

Atrial fibrillation is a disorder in which the atria beat in a rapid and irregular manner. This chaotic automatic firing affects all excitable structures in the atrium, including the sinus node and the AV node. Due to a remodeling of ion channels in these excitable structures, atrial fibrillation episodes may be followed by asystole. If the sinus node is already impaired by ischemia, inflammation, or chronic volume or pressure overload, the probability of clinically relevant pauses increases. If pauses cause symptoms or exceed a defined length, an artificial pacemaker should be considered.

Bradycardia tachycardia syndrome is the combination of sinus node pathology and paroxysmal atrial fibrillation with tachycardia.

Two mechanisms are responsible for the maintenance of the typical changing rhythms and heart rates.

1. Atrial fibrillation leads to continuous depolarization of the sinus node and the AV node. This "automatic fire" results in pre-automatic pauses and bradycardic episodes.

2. During the bradycardic episodes, supraventricular premature beats often occur. These may in turn trigger atrial fibrillation or other atrial tachycardias.

Frequently, control of the tachycardia by medication is impossible, due to the overwhelmingbradycardiac effect of antiarrhythmic agents. In addition to the performance of invasive procedures, the disorder can be controlled using pacemaker implantation and the prescription of medication to lower the heart rate. In extreme cases, a "pace-and-ablate" approach, involving the complete ablation of the AV-node, may be considered.