Essential Cardiac Electrophysiology

Before basic ECG patterns are discussed, we will review a few simple principles of the heart’s electrical properties.

The central function of the heart is to contract rhythmically and pump blood to the lungs for oxygenation and then to pump this oxygen-enriched blood into the general (systemic) circulation.

The signal for cardiac contraction is the spread of electrical currents through the heart muscle. These currents are produced both by pacemaker cells and specialized conduction tissue within the heart and by the working heart muscle itself.

Pacemaker cells are like tiny clocks (technically called oscillators) that repetitively generate electrical stimuli. The other heart cells, both specialized conduction tissue and working heart muscle, are like cables that transmit these electrical signals.

Electrical Activation of the Heart

In simplest terms, therefore, the heart can be thought of as an electrically timed pump. The electrical “wiring” is outlined in Figure 1-1.

Figure 1-1 Normally, the cardiac stimulus is generated in the sinoatrial (SA) node, which is located in the right atrium (RA). The stimulus then spreads through the RA and left atrium (LA). Next, it spreads through the atrioventricular (AV) node and the bundle of His, which compose the AV junction. The stimulus then passes into the left and right ventricles (LV and RV) by way of the left and right bundle branches, which are continuations of the bundle of His. Finally, the cardiac stimulus spreads to the ventricular muscle cells through the Purkinje fibers.

Normally, the signal for heartbeat initiation starts in the sinus or sinoatrial (SA) node. This node is located in the right atrium near the opening of the superior vena cava. The SA node is a small collection of specialized cells capable of automatically generating an electrical stimulus (spark-like signal) and functions as the normal pacemaker of the heart. From the sinus node, this stimulus spreads first through the right atrium and then into the left atrium.

Electrical stimulation of the right and left atria signals the atria to contract and pump blood simultaneously through the tricuspid and mitral valves into the right and left ventricles. The electrical stimulus then reaches specialized conduction tissues in the atrioventricular (AV) junction.

The AV junction, which acts as an electrical “relay” connecting the atria and ventricles, is located at the base of the interatrial septum and extends into the interventricular septum (see Fig. 1-1).

The upper (proximal) part of the AV junction is the AV node. (In some texts, the terms AV node and AV junction are used synonymously.)

The lower (distal) part of the AV junction is called the bundle of His. The bundle of His then divides into two main branches: the right bundle branch, which distributes the stimulus to the right ventricle, and the left bundle branch,^† which distributes the stimulus to the left ventricle (see Fig. 1-1).

The electrical signal then spreads simultaneously down the left and right bundle branches into the ventricular myocardium (ventricular muscle) by way of specialized conducting cells called Purkinje fibers located in the subendocardial layer (inside rim) of the ventricles. From the final branches of the Purkinje fibers, the electrical signal spreads through myocardial muscle toward the epicardium (outer rim).

The His bundle, its branches, and their subdivisions are referred to collectively as His-Purkinje system. Normally, the AV node and His-Purkinje system form the only electrical connection between the atria and the ventricles (unless a bypass tract is present; see Chapter 12). Disruption of conduction over these structures will produce AV heart block (Chapter 17).

Just as the spread of electrical stimuli through the atria leads to atrial contraction, so the spread of stimuli through the ventricles leads to ventricular contraction, with pumping of blood to the lungs and into the general circulation.

The initiation of cardiac contraction by electrical stimulation is referred to as electromechanical coupling. A key part of this contractile mechanism is the release of calcium ions inside the atrial and ventricular heart muscle cells, which is triggered by the spread of electrical activation. This process links electrical and mechanical function.

The ECG is capable of recording only relatively large currents produced by the mass of working (pumping) heart muscle. The much smaller amplitude signals generated by the sinus node and AV node are invisible with clinical recordings. Depolarization of the His bundle area can only be recorded from inside the heart during specialized cardiac electrophysiologic (EP) studies.

Cardiac Automaticity and Conductivity: “Clocks and Cables”

Automaticity refers to the capacity of certain cardiac cells to function as pacemakers by spontaneously generating electrical impulses, like tiny clocks. As mentioned earlier, the sinus node normally is the primary (dominant) pacemaker of the heart because of its inherent automaticity.

Under special conditions, however, other cells outside the sinus node (in the atria, AV junction, or ventricles) can also act as independent (secondary) pacemakers. For example, if sinus node automaticity is depressed, the AV junction can act as a backup (escape) pacemaker. Escape rhythms generated by subsidiary pacemakers provide important physiologic redundancy (safety mechanism) in the vital function of heartbeat generation.

Normally, the relatively more rapid intrinsic rate of SA node firing suppresses the automaticity of these secondary (ectopic) pacemakers outside the sinus node. However, sometimes, their automaticity may be abnormally increased, resulting in competition with the sinus node for control of the heartbeat. For example, a rapid run of ectopic atrial beats results in atrial tachycardias (Chapter 14). A rapid run of ectopic ventricular beats results in ventricular tachycardia (Chapter 16), a potentially life-threatening arrhythmia.

In addition to automaticity, the other major electrical property of the heart is conductivity. The speed with which electrical impulses are conducted through different parts of the heart varies. The conduction is fastest through the Purkinje fibers and slowest through the AV node. The relatively slow conduction speed through the AV node allows the ventricles time to fill with blood before the signal for cardiac contraction arrives. Rapid conduction through the His-Purkinje system ensures synchronous contraction of both ventricles.

If you understand the normal physiologic stimulation of the heart, you have the basis for understanding the abnormalities of heart rhythm and conduction and their distinctive ECG patterns. For example, failure of the sinus node to effectively stimulate the atria can occur because of a failure of SA automaticity or because of local conduction block that prevents the stimulus from exiting the sinus node. Either pathophysiologic mechanism can result in apparent sinus node dysfunction and sometimes symptomatic sick sinus syndrome (Chapter 20). These patients may experience lightheadedness or even syncope (fainting) because of marked bradycardia (slow heartbeat).

In contrast, abnormal conduction within the heart can lead to various types of tachycardia due to reentry, a mechanism in which an impulse “chases its tail,” short-circuiting the normal activation pathways. Reentry plays an important role in the genesis of paroxysmal supraventricular tachycardias (PSVTs), including those involving a bypass tract, as well as in many ventricular tachycardias.

Blockage of the spread of stimuli through the AV node or infranodal pathways can produce various degrees of AV heart block (Chapter 17), sometimes with severe, symptomatic ventricular bradycardia, necessitating placement of a temporary or permanent placement pacemaker.

Disease of the bundle branches, themselves, can produce right or left bundle branch block (resulting in electrical dyssynchrony, an important contributing mechanism in many cases of heart failure; see Chapters 7 and 21).

Preview: Looking Ahead

The first part of this book is devoted to explaining the basis of the normal ECG and then examining the major conditions that cause abnormal depolarization (P and QRS) and repolarization (ST-T and U) patterns. This alphabet of ECG terms is defined in Chapter 2.

The second part deals with abnormalities of cardiac rhythm generation and conduction that produce excessively fast or slow heart rates (tachycardias and bradycardias).

The third part provides both a review and important extension of material covered in earlier chapters, including a focus on avoiding ECG errors.

Selected publications are cited in the Bibliography, including freely available online resources. In addition, the online supplement to this book provides extra material, including numerous case studies.

Concluding Notes: Why is the ECG So Clinically Useful?

The ECG is one of the most versatile and inexpensive of clinical tests. Its utility derives from careful clinical and experimental studies over more than a century showing the following: