Which of the following is the most reliable method of estimating a patient in cardiac output?

A typical electrocardiographic record is indicated in Figure 4–2. The major features of the electrocardiogram are the P, QRS, and T waves that are caused by atrial depolarization, ventricular depolarization, and ventricular repolarization, respectively. The period from the initiation of the P wave to the beginning of QRS complex is designated as the PR interval and indicates the time it takes for an action potential to spread through the atria and the atrioventricular (AV) node. During the latter portion of the PR interval (PR segment), no voltages are detected on the body surface. This is because atrial muscle cells are depolarized (in the plateau phase of their action potentials), ventricular cells are still resting, and the electrical field set up by the action potential progressing through the small AV node is not intense enough to be detected. The duration of the normal PR interval ranges from 120 to 200 ms. Shortly after the cardiac impulse breaks out of the AV node and into the rapidly conducting Purkinje system, all the ventricular muscle cells depolarize within a very short period and cause the QRS complex. The R wave is the largest event in the electrocardiogram because ventricular muscle cells are numerous and they depolarize nearly in unison. The normal QRS complex lasts between 60 and 100 ms. (The repolarization of atrial cells also occurs during the period in which ventricular depolarization generates the QRS complex on the electrocardiogram (see Figure 2–5). Atrial repolarization is not evident on the electrocardiogram because it is a poorly synchronized event in a relatively small mass of heart tissue and is completely overshadowed by the major electrical events occurring in the ventricles at this time.)

Figure 4–2.

Typical electrocardiogram of a single cardiac cycle.

The QRS complex is followed by the ST segment. Normally, no electrical potentials are measured on the body surface during the ST segment because no rapid changes in membrane potential are occurring in any of the cells of the heart; atrial cells have already returned to the resting phase, whereas ventricular muscle cells are in the plateau phase of their action potentials. (Myocardial injury or inadequate blood flow, however, can produce elevations or depressions in the ST segment.) When ventricular cells begin to repolarize, a voltage difference once again appears on the body surface and is measured as the T wave of the electrocardiogram. The T wave is broader and not as large as the R wave because ventricular repolarization is less synchronous than depolarization. At the conclusion of the T wave, all the cells in the heart are in the resting state. The QT interval roughly approximates the duration of ventricular myocyte action potential and thus the period of ventricular systole. At a normal heart rate of 60 beats/min, the QT interval is normally less than 380 ms. No body surface potential is measured until the next impulse is generated by the sinoatrial (SA) node.

It should be recognized that the operation of the specialized conduction system is a primary factor in determining the normal electrocardiographic pattern. For example, the AV nodal transmission time determines the PR interval. Also, the effectiveness of the Purkinje system in synchronizing ventricular depolarization is reflected in the large magnitude and short duration of the QRS complex. It should also be noted that nearly every heart muscle cell is inherently capable of rhythmicity and that all cardiac cells are electrically interconnected through gap junctions. Thus, a functional heart rhythm can, and often does, occur without the involvement of part or all of the specialized conduction system. Such a situation is, however, abnormal, and the existence of abnormal conduction pathways would produce an abnormal electrocardiogram.

Basic Electrocardiographic Conventions

Recording electrodes are placed on both arms and the left leg—usually at the wrists and the ankle. The appendages are assumed to act merely as extensions of the recording system, and voltage measurements are assumed to be made between points that form an equilateral triangle over the thorax, as shown in Figure 4–3. This conceptualization is called Einthoven’s triangle in honor of the Dutch physiologist who devised it in the early 20th century. Any single electrocardiographic trace is a recording of the voltage difference measured between any 2 vertices of Einthoven’s triangle. An example of the lead II electrocardiogram measured between the right arm and the left leg has already been shown in Figure 4–2. Similarly, lead I and lead III electrocardiograms represent voltage measurements taken along the other two sides of Einthoven’s triangle, as indicated in Figure 4–3. The “+” and “-” symbols in Figure 4–3 indicate polarity conventions that have been universally adopted. For example, an upward deflection in a lead II electrocardiogram (as normally occurs during the P, R, and T waves) indicates that an electrical potential exists at that instant between the left leg and the right shoulder electrodes, with the left leg electrode being positive. Conversely, a downward deflection in a lead II record indicates that a polarity exists between the electrodes at that instant, with the left leg electrode being negative. Similar polarity conventions have been established for lead I and lead III recordings and are indicated by the “+” and “-” symbols in Figure 4–3. In addition, electrocardiographic recording equipment is often standardized so that a 1-cm deflection on the vertical axis always represents a potential difference of 1 mV, and that 25 mm on the horizontal axis of any electrocardiographic record represents 1 s. Most electrocardiographic records contain calibration signals so that abnormal rates and wave amplitudes can be easily detected.

Figure 4–3.

Einthoven’s electrocardiographic conventions.

As shown in the next chapter, many cardiac electrical abnormalities can be detected in recordings from a single electrocardiographic lead. However, certain clinically useful information can be derived only by combining the information obtained from two electrocardiographic leads. To understand these more complex electrocardiographic analyses, a close examination of how voltages appear on the body surface as a result of the cardiac electrical activity must be done.

Cardiac Dipoles and Electrocardiographic Records

Figure 4–4.

Net cardiac dipole during atrial depolarization and its components on the limb leads.

The net dipole that exists at any instant during depolarization is oriented (ie, points) in the general direction of wavefront movement at that instant. The magnitude or strength of the dipole (represented here by the arrow length) is determined by (1) how extensive the wavefront is (ie, how many cells are simultaneously depolarizing at the instant in question) and (2) the consistency of orientation between individual dipoles at different points in the wavefront (dipoles with the same orientation reinforce each other; dipoles with the opposite orientation cancel each other).

The net dipole in the example in Figure 4–4 causes the lower-left portion of the body to be generally positive with respect to the upper-right portion. This particular dipole will cause positive voltages to exist on all three of the electrocardiogram limb leads. As shown in the right half of Figure 4–4, this can be deduced from Einthoven’s triangle by observing that the net dipole has some component that points in the positive direction of leads I, II, and III. As illustrated in Figure 4–4, the component that a cardiac dipole has on a given electrocardiogram lead is found by drawing perpendicular lines from the appropriate side of Einthoven’s triangle to the tip and tail of the dipole. (It may be helpful to think of the component on each lead as the “shadow” cast by the dipole on that lead as a result of a “sun” located far beyond the corner of Einthoven’s triangle that is opposite the lead.) Note that the dipole in this example is most parallel to lead II and therefore has a large component in the lead II direction. Thus, it will create a larger voltage on lead II than on lead I or lead III. This dipole has a rather small component on lead III because it is oriented nearly perpendicular to lead III.

The limb lead configuration may be thought of as a way to view the heart’s electrical activity from three different perspectives (or axes). The vector representing the heart’s instantaneous dipole strength and orientation is the object under observation, and its appearance depends on the position from which it is viewed. The instantaneous voltage measured on the axis of lead I, for example, indicates how the dipole being generated by the heart’s electrical activity at that instant appears when viewed from directly above. A cardiac dipole that is oriented horizontally appears large on lead I, whereas a vertically oriented cardiac dipole, however large, produces no voltage on lead I. Thus, it is necessary to have views from 2 directions to establish the magnitude and orientation of the heart’s dipole. A vertically oriented dipole would be invisible on lead I but would be readily apparent if viewed from the perspective of lead II or lead III.

It is important to emphasize that the example in Figure 4–4 pertains only to one instant during atrial depolarization. The net cardiac dipole continually changes in magnitude and orientation during the course of atrial depolarization. The nature of these changes will determine the shape of the P wave on each of the electrocardiogram leads.

The P wave terminates when the wave of depolarization, as illustrated in Figure 4–4, reaches the nonmuscular border between the atria and the ventricles and the number of individual dipoles becomes very small. At this time, the cardiac impulse is still being slowly transmitted toward the ventricles through the AV node. However, the electrical activity in the AV node involves so few cells that it generates no detectable net cardiac dipole. Thus, no voltages are measured on the surface of the body for a brief period following the P wave. A net cardiac dipole reappears only when the depolarization completes its passage through the AV node, enters the Purkinje system, and begins its rapid passage over the ventricular muscle cells. Because the Purkinje fibers initially pass through the intraventricular septum and to the endocardial layers at the apex of the ventricles, ventricular depolarization occurs first in these areas and then proceeds outward and upward through the ventricular myocardium.

Ventricular Depolarization and the QRS Complex

It is the rapid and large changes in the magnitude and direction of the net cardiac dipole that occur during ventricular depolarization that cause the QRS complex of the electrocardiogram. The normal process is illustrated in Figure 4–5. The initial ventricular depolarization usually occurs on the left side of the intraventricular septum, as illustrated in the upper panel of the figure. Analysis of the cardiac dipole formed by this initial ventricular depolarization with the aid of Einthoven’s triangle shows that this dipole has a negative component on lead I, a small negative component on lead II, and a positive component on lead III. The upper-right panel shows the actual deflections on each of the electrocardiographic limb leads that will be produced by this dipole. Note that it is possible for a given cardiac dipole to produce opposite deflections on different leads. For example, in Figure 4–5, Q waves appear on leads I and II but not on lead III.

Figure 4–5.

Ventricular depolarization and the generation of the QRS complex.

The second row of panels in Figure 4–5 shows the ventricles during the instant in ventricular depolarization when the number of individual dipoles is greatest and/or their orientation is most similar. This phase generates the large net cardiac dipole, which is responsible for the R wave of the electrocardiogram. In Figure 4–5, this net cardiac dipole is nearly parallel to lead II. As indicated, such a dipole produces large positive R waves on all three limb leads.

The third row in Figure 4–5 shows the situation near the end of the spread of depolarization through the ventricles and indicates how the small net cardiac dipole present at this time produces the S wave. Note that an S wave does not necessarily appear on all electrocardiogram leads (as in lead I of this example).

The bottom row in Figure 4–5 shows that during the ST segment, all ventricular muscle cells are in a depolarized state. There are no waves of electrical activity moving through the heart tissue. Consequently, no net cardiac dipole exists at this time and no voltage differences exist between points on the body surface. All electrocardiographic traces will be flat at the isoelectric (zero voltage) level.

Ventricular Repolarization and the T Wave

As illustrated in Figure 4–2, the T wave is normally positive on lead II as is the R wave. This indicates that the net cardiac dipole generated during ventricular repolarization is oriented in the same general direction as that existing during ventricular depolarization. This may be somewhat surprising. However, recall from Figure 2–5 that the last ventricular cells to depolarize are the first to repolarize. The reasons for this are not well understood, but the result is that the wavefront of electrical activity during ventricular repolarization tends to retrace, in reverse direction, the course followed during ventricular depolarization. Therefore, the dipole formed during repolarization has the same polarity as that during depolarization. This reversed wavefront propagation pathway during ventricular repolarization results in a positive T wave recorded, for example, on lead II. The T wave is broader and smaller than the R wave because the repolarization of ventricular muscle cells is less well synchronized than is their depolarization.

Mean Electrical Axis and Axis Deviations

Figure 4–6.

Mean electrical axis and axis deviations.

The mean electrical axis of the heart can be determined from the electrocardiogram. The process involves determining what single net dipole orientation will produce the R-wave amplitudes recorded on any two leads. For example, if the R waves on leads II and III are both positive (upright) and of equal magnitude, the mean electrical axis must be +90 degrees. As should be obvious, in this case, the amplitude of the R wave on lead I will be zero.1 Alternatively, one can scan the electrocardiographic records for the lead tracing with the largest R waves and then deduce that the mean electrical axis must be nearly parallel to that lead. In Figure 4–5, for example, the largest R wave occurs on lead II. Lead II has an orientation of +60 degrees, which is very close to the actual mean electrical axis in this example.

Another analysis technique called vectorcardiography is based on continuously following the magnitude and orientation of the heart’s dipole throughout the cardiac cycle. A typical vectorcardiogram is illustrated in Figure 4–7 and is a graphical record of the dipole amplitude in the x and y directions throughout a single cardiac cycle. If one imagines the heart’s electrical dipole as a vector with its tail always positioned at the center of Einthoven’s triangle, then the vectorcardiogram can be thought of as a complete record of all the various positions that the head of the dipole assumes during the course of one cardiac cycle. A vectorcardiogram starts from an isoelectric diastolic point and traces three loops during each cardiac cycle. The first small loop is caused by atrial depolarization, the second large loop is caused by ventricular depolarization, and the final intermediate-sized loop is caused by ventricular repolarization. The mean electrical axis of the ventricle is immediately apparent in a vectorcardiographic record as the orientation of the largest deviation from the isoelectric point during ventricular depolarization. Analogous “mean axes” can similarly be defined for the P wave and T wave but are not commonly used.

Figure 4–7.

Typical vectorcardiogram.

The Standard 12-Lead Electrocardiogram

The standard limb leads (I, II, and III) and the augmented unipolar limb leads (aVR, aVL, and aVF) record the electrical activity of the heart as it appears from 6 different “perspectives,” all in the frontal plane. As shown in Figure 4–8A, the axes for leads I, II, and III are those of the sides of Einthoven’s triangle, whereas those for aVR, aVL, and aVF are specified by lines drawn from the center of Einthoven’s triangle to each of its vertices. As indicated in Figure 4–8B, these 6 limb leads can be thought of as a hexaxial reference system for observing the cardiac vectors in the frontal plane.

Figure 4–8.

The standard 12-lead electrocardiogram. (A and B) Leads in the frontal plane. (C) Electrode positions for precordial leads in the transverse plane.

The other 6 leads of the standard 12-lead electrocardiogram are also unipolar leads that “look” at the electrical vector projections in the transverse plane. These potentials are obtained by placing an additional (exploring) electrode in 6 specified positions on the chest wall, as shown in Figure 4–8C. The indifferent electrode in this case is formed by electrically connecting the limb electrodes. These leads are identified as precordial or chest leads and are designated as V1 through V6. As shown in this figure, when the positive electrode is placed in position 1 and the wave of ventricular excitation sweeps away from it, the resultant deflection will be downward. When the electrode is in position 6 and the wave of ventricular excitation sweeps toward it, the deflection will be upward.

In summary, the electrocardiogram is a powerful tool for evaluating cardiac excitation characteristics. It must be recognized, however, that the ECG does not provide direct evidence of mechanical pumping effectiveness. For example, a leaky valve will have no direct electrocardiographic consequences but may adversely influence pumping ability of the heart.

1 An accurate, albeit tedious, way to determine the mean electrical axis is to follow these steps: (1) determine the algebraic sum of the R- and S-wave amplitude on each of the two leads, (2) plot these magnitudes as components on the appropriate sides of Einthoven’s equilateral triangle according to the standardized polarity conventions, (3) project perpendicular lines from the heads and tails of these components into the interior of the triangle to find the position of the head and tail of the cardiac dipole, which produced the R waves, and (4) measure the angular orientation of this dipole.

Which of the following is the most reliable method of estimating a patient's cardiac output group of answer choices?

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