Electrocardiogram

1

Describe the electrical conduction system of the heart.

The electrical conduction system of the heart is a network of specialized myocardial cells that generate, regulate, and propagate a series of electrical impulses. These impulses are generated by subtle changes in the resting membrane potential because of the movement of ions through cellular membrane channels.

The basic structure of this system consists of specialized cells that make up the sinoatrial (SA) node, the atrioventricular (AV) node, the His bundle, the left and right bundles, and the Purkinje fibers (PF).

The SA node is located within the wall of the RA. It has an unstable resting potential (discussed later), allowing it to spontaneously generate electrical activity that is propagated via specialized atrial cells known as the internodal tract to the AV node . The AV node acts as a “gate-keeper” by regulating a small delay before the electrical signal can propagate to the very efficient His-bundle-PF system.

The purpose of the electrical conduction system is to coordinate contraction between all four chambers of the heart to efficiently generate a stroke volume. Disorders that impair the electrical conduction system, such as AV node block, left bundle branch block (LBBB), or atrial fibrillation, cause mechanical dyssynchrony between the chambers of the heart and impair cardiac output.

2

What is unique about the action potential at the SA node (and other pacemaker cells)?

The SA node is unique in that it can spontaneously depolarize because of inward sodium “funny” current ( Fig. 28.1 ). This “funny” current allows the SA node to have automaticity where it can spontaneously depolarize at an intrinsic rate. Although the SA node is the primary pacemaker for the heart, cells in the AV node and PF also have “funny” current giving them automaticity as well although at a slower rate. The following are the phases for an SA node action potential:

• Phase 4 : Slowly depolarizes automatically because of an inward Na ⁺ current called funny current. It is called funny current because this ion channel is activated by negative membrane potentials (hyperpolarization), which contrasts other ion channels, which are activated by positive membrane potentials (depolarization). Pacemaker cells, such as the SA node, contain the property described in this phase because it allows for spontaneous depolarization.

• Phase 0 : After a certain membrane potential is reached, the upstroke of the action potential is generated by voltage-gated Ca ^{2 +} channel opening causing an increase of inward Ca ^{2 +} current.

• Phase 3 : The repolarization phase is caused by inactivation of Ca ^{2 +} channels and K ⁺ current out of the cell.

3

How is the action potential of the atrial and ventricular myocytes different than the SA node?

In addition to the funny current giving the SA node automaticity, the SA node only has three phases, whereas the atrial and ventricular myocyte actional potential has five phases (see Fig. 28.1 ) as depicted later:

• Phase 0 : This is the upstroke of the action potential, but here, it is caused by opening of voltage-gated Na ⁺ channels, which depolarize the membrane.

• Phase 1 : The rapid depolarization from phase 0, causes a small overshoot in depolarization, which is corrected by a small repolarization because of a decrease in inward Na ⁺ current and an increase in K ⁺ current out of the cell.

• Phase 2 : The plateau of the action potential is maintained by an increase in Ca ^{2 +} current into the cell and by an outward K ⁺ current. The plateau marks a period of dynamic equilibrium of inward and outward cation currents.

• Phase 3 : Repolarization is caused by a predominance of outward K ⁺ current and inactivation of calcium channels. This hyperpolarizes the membrane.

• Phase 4 : The cell is hyperpolarized and is at its resting membrane potential. This reflects a state where a dynamic equilibrium exists between all permeable ions.

4

So, if the SA node fails, what keeps the heart beating then?

Phase 4 depolarization automaticity (just like the SA node) also occurs within the AV node and the PF, albeit at a slower (usually much slower) rate of depolarization. Therefore if there is suppression of the SA node or its signal propagation, these specialized cells can act as the de facto pacemaker of the heart. Therefore patients who lack a functioning SA or AV node (sick sinus syndrome, complete heart block, etc.) will continue to have a heartbeat and can survive until a permanent pacemaker is placed. The automaticity of the AV node is about 40 to 60 beats per minute and for the PF, 30 to 40 beats per minute.

5

Explain how an electrocardiogram is obtained from a patient.

The electrical conduction system of the heart produces small voltage changes that can be measured by attaching electrodes to the body. The electrodes transmit this electrical signal to an electrocardiogram (ECG) machine that filters noise and amplifies the small voltage to a larger voltage, so we can visualize the electrical activity of the heart. Furthermore, when electrodes are placed in standardized locations across the body, we can understand the electrical potential differences of the heart that is conducive to systematic study and clinical interpretation. In other words, we use the electrodes to monitor the direction of electrical signals emitted by the heart to diagnose and treat problems.

6

What are the customary lead placements sites for a 12-lead ECG?

A standard 12-lead ECG contains 10 electrodes. The four limb electrodes correspond to each limb (right arm, left arm, right leg, left leg) and measure the ECG voltage changes in the frontal axis. The six precordial leads are placed across the chest from the sternum to the left axilla and measure ECG changes in the transverse axis. Please see Fig. 28.2 .

7

Why are there are only 10 electrodes, but 12 leads?

There are four limb electrodes (right arm, left arm, right leg, and left leg) and six precordial electrodes (V1–V6). These 10 electrodes create nine axes (three limb axes and six precordial axes) and the last electrode (right leg) serves as a ground. Each axis measures the projected electric field force generated by the atria (P wave) and ventricles (QRS and T waves). The remaining three leads are “virtual” axes created by combining two electrodes to create a new virtual ground that can be used to create an “augmented” axis (i.e., aVR, aVF, aVL).

8

Describe the limb leads.

The limb leads measure ECG voltage differences across the frontal plane of the heart:

• Lead I measures the voltage difference between the left arm (LA) and the right arm (RA) electrode: Lead I = LA – RA.

• Lead II measures the voltage difference between the left leg (LL) and the right arm (RA) electrode: Lead II = LL – RA.

• Lead III measures the voltage difference between the left leg (LL) and the left arm (LA) electrode: Lead III = LL – LA.

9

What is the Wilson central terminal?

The Wilson central terminal (WCT) is a virtual electrode that is used as a reference point for the augmented limb and precordial leads. It is determined by summing the three limb electrodes and averaging their voltage: $\mathrm{WCT}=\frac{\mathrm{LA}+\mathrm{RA}+\mathrm{LL}}{3}$ . The WCT mathematically represents a central “virtual” electrode at the center of Einthoven’s triangle.

10

Describe the precordial leads.

The precordial leads measure ECG voltage differences across the transverse plane of the heart. It consists of six “virtual” axes created by six “positive” electrodes that surround the chest where each electrode uses the virtual WCT as its “negative” reference electrode. Each of the six precordial leads, just like the limb leads, measure the heart’s electric field force (a vector) projected onto an axis. Each precordial axis is referred to as V _i , where “i” represents the six precordial electrodes. Each precordial lead or axis can be calculated as follows:

V _i , precordial voltage lead; φ _i , precordial electrode; WCT, Wilson central terminal; i, corresponding lead/electrode 1 to 6

Note that some texts refer to the precordial leads as unipolar , implying these leads do not require a negative electrode. However, that is false; all ECG leads represent the difference between a positive and negative electrode, whether created virtually by combing multiple electrodes together or by using one single electrode. Lastly, “V” is abbreviated notation for both precordial and augmented leads and may refer to virtual, vector, or voltage.

11

Describe the augmented leads.

The three remaining leads are the augmented voltage (aV) left, right, and foot leads:

• aVL is the voltage difference between the LA electrode and the average voltage of the RA and LL electrodes: $\mathrm{aVL}=\mathrm{LA}-\frac{\mathrm{RA}+\mathrm{LL}}{2}$

• aVR is the voltage difference between the RA electrode and the average voltage of the LL and LA electrodes: $\mathrm{aVR}=\mathrm{RA}-\frac{\mathrm{LL}+\mathrm{LA}}{2}$

• aVF is the voltage difference between the LL electrode and the average voltage of the RA and LA electrodes: $\mathrm{aVF}=\mathrm{LL}-\frac{\mathrm{RA}+\mathrm{LA}}{2}$

12

Why are “augmented leads” augmented? Is this necessary?

Originally, these leads were simply referred to as VL, VR, and VF with the same negative virtual electrode, WCT, as the precordial leads. For example, $\mathrm{VL}=\mathrm{LA}-\frac{\mathrm{RA}+\mathrm{LL}+\mathrm{LA}}{3}$ . Unfortunately, the amplitude of the ECG voltage measured on these leads was found to be too small with a low signal-to-noise ratio. To increase the voltage and improve the signal-to-noise ratio, it was found that the voltage of these leads could be “augmented” by using a different virtual negative electrode. Instead of using WCT, all ECG machines today use the average of the two opposite electrodes (i.e., Goldberger’s central terminal) and not all three electrodes as in WCT. It is important to emphasize that this was first proposed and implemented in the 1940s, way before digital amplifiers even existed. With current high-fidelity digital amplifiers and filters, a strong argument can be made that voltage augmentation of limb leads using mathematical “trickery” (i.e., Goldberg’s central terminal) is no longer necessary and that we should return back to WCT as the reference virtual electrode, so these leads can share the same virtual electrode as the precordial leads. Regardless, the effects on Einthoven’s triangle in determining axis projection and angles between vectors is unaffected, regardless of which virtual electrode implementation is used.

13

What are the waveforms of a normal ECG?

Please refer to Figure 28.3 . It is important to understand that electrical activity on ECG does not imply simultaneous mechanical contraction. There is a small latency between the electrical activity detected on ECG and mechanical contraction of the heart.

The P wave is the first upward (positive) deflection during the cardiac cycle, demonstrating atrial depolarization. It is a combination of, first, right atrial, then, left atrial depolarization. Any downward deflection following the P wave that precedes the R wave is considered a Q wave . The Q wave represents depolarization of the interventricular septum, which occurs from left to right. Presumably, this is because the electrical conduction velocity of the left heart is slightly faster than the right heart, allowing the larger left heart to contract in synchrony with the smaller right heart. The R wave is the first upward (positive) deflection of the QRS complex or the first upward deflection after a P wave . It signals early ventricular depolarization. The S wave is the first downward (negative) deflection of the QRS complex, which occurs after the R wave . It is caused by late ventricular depolarization from the PF. The ST segment is normally not elevated and isoelectric starting at the J point to the beginning of the T wave . The T wave is the upward (positive) deflection after a QRS complex . It is caused by ventricular repolarization and is normally upright (positive) in all leads except aVR.

14

What is the “J point”?

The J point is the junction between the end of the QRS complex and the beginning of the ST segment. This transition point usually occurs at the isoelectric point on the ECG, but deviations above or below the isoelectric point may reflect pathology. Elevated J point is thought to reflect early depolarization. Most often, it is seen in young, healthy, athletic males and is traditionally thought to be benign in the acute setting. However, there is some evidence to suggest a higher incidence of sudden cardiac death and Brugada syndrome in patients with elevated J point.

15