Anatomic Orientation of the Heart Within the Body

The position of the heart within the body determines the “view” of the cardiac electrical activity that can be observed from any ECG recording electrode site on the body surface. The atria are located in the top or base of the heart, and the ventricles taper toward the bottom or apex. However, the right and left sides of the heart are not directly aligned with the right and left sides of the body. The long axis of the heart, which extends from base to apex, is tilted to the left and anteriorly at its apical end (Figure 10-5). Also, the heart is rotated so that the right atrium and ventricle are more anterior than the left atrium and ventricle.^8,9 These anatomic relationships dictate that an ECG lead providing a right anterior to left posterior view (such as V1) provides better differentiation of right versus left cardiac activity than does a lead providing a right lateral to left lateral view (such as lead I) (Figure 10-6).

FIGURE 10-5 The schematic frontal-plane view of the heart in the thorax with electrodes, where the long axis intersects with the body surface. The positive electrode on the left lower thoracic wall and the negative electrode on the right shoulder are aligned from the cardiac base to apex parallel to the inter-atrial and interventricular septa and are attached to a single-channel electrocardiogram recorder. The ventricular repolarization wave is positively oriented. L, Left; R, right.

FIGURE 10-6 The schematic transverse-plane view of the heart in the thorax with electrodes, where the short axis intersects with the body surface. The positive electrode to the right of the sternum and the negative electrode on the back are aligned perpendicular to the inter-atrial and interventricular septa and are attached to a single-channel electrocardiogram recorder. The typically diphasic P and T waves and the predominately negative QRS complex recorded by electrodes at these positions are indicated on the electrocardiogram. LA, Left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

The Cardiac Cycle

The timing and synchronization of contraction of myocardial cells are controlled by cells of the pacemaking and conduction system. Impulses generated within these cells create a rhythmic repetition of events called cardiac cycles. Each cycle is composed of electrical and mechanical activation (systole) and recovery (diastole). Since the electrical events initiate the mechanical events, a brief delay occurs between the onsets of electrical and mechanical systole and of electrical and mechanical diastole.

The electrical recording from inside a single myocardial cell as it progresses through a cardiac cycle is illustrated in the top panel of Figure 10-7. During electrical diastole, the cell has a baseline negative electrical potential and is also in mechanical diastole with separation of its contractile proteins. An electrical impulse arriving at the cell allows positively charged ions to cross the cell membrane, causing its depolarization. This movement of ions initiates electrical systole, which is characterized by an action potential (see Figure 10-7, middle panel). This electrical event then initiates mechanical systole, in which the contractile proteins slide over each other, thereby shortening the cell. Electrical systole continues until the positively charged ions are pumped out, causing repolarization of the cell. The electrical potential returns to its negative resting level. This return of electrical diastole causes the contractile proteins to separate again. The cell is then capable of being reactivated if another electrical impulse arrives at its membrane.

FIGURE 10-7 The schematic electrocardiogram recording beneath a cardiac cellular action potential.

(Modified from Thaler MS: The Only EKG book you’ll ever need, Philadelphia, 1988, JB Lippincott, p 11.)

The ECG recording is formed by the summation of electrical signals from all of the myocardial cells (see Figure 10-7, lower panel). When the cells are in their resting state, the ECG recording produces a flat baseline. The onset of depolarization of the cells produces a relatively high-frequency ECG waveform. Then, while depolarization persists, the ECG returns to the baseline. Repolarization of the myocardial cells is represented on the ECG by a lower frequency waveform in the opposite direction from that representing depolarization.

Cardiac Impulse Formation and Conduction

The electrical activation of a single cardiac cell or even a small group of cells does not produce enough current to be recorded on the body surface. Clinical electrocardiography is made possible by the activation of atrial and ventricular myocardial masses that are of sufficient magnitude for their electrical activity to be recorded on the body surface.

Myocardial cells normally lack the ability for either spontaneous formation or rapid conduction of an electrical impulse. They are dependent for these functions on specialized (Purkinje) cells of the cardiac pacemaking and conduction system placed strategically through the heart (Figure 10-8). These cells are arranged in nodes, bundles, bundle branches, and branching networks of fascicles. They lack contractile capability but are able to achieve spontaneous electrical impulse formation (acting as pacemakers) and to alter the speed of electrical conduction. The intrinsic pacemaking rate is most rapid in the specialized cells in the sinus node and slowest in the specialized cells in the ventricles. The intrinsic pacing rate is altered by the balance between the sympathetic and parasympathetic components of the autonomic nervous system.^10–13

FIGURE 10-8 Three views of the anatomic relationships among the cardiac pumping chambers and the structures of the pacemaking and conduction system. A, From the anterior precordium. B, From the right anterior precordium looking onto the inter-atrial and interventricular septa through the right atrium and ventricle. C, From the left posterior thorax looking onto the septa through the left atrium and ventricle. AV, Atrioventricular; SA, sinoatrial.

(Modified from Netter FH: The Ciba collection of medical illustrations, vol 5. In Yonkman FF, editor: Heart, Summit, NJ, 1978, Ciba-Geigy, pp 13, 49.)

The intraventricular conduction pathways include a common bundle (bundle of His), leading from the atrioventricular (AV) node to the summit of the interventricular septum, and its right and left bundle branches, proceeding along the septal surfaces to their respective ventricles (see Figure 10-8, A). The left bundle branch fans into fascicles that proceed along the left septal surface and toward the two papillary muscles of the mitral valve (see Figure 10-8, B). The right bundle branch remains compact until it reaches the right distal septal surface, where it branches into the distal interventricular septum and toward the lateral wall of the right ventricle (see Figure 10-8, C). These intraventricular conduction pathways are composed of fibers of Purkinje cells with specialized capabilities for both pacemaking and rapid conduction of electrical impulses. Fascicles composed of Purkinje fibers form networks that extend just beneath the surface of the right and left ventricular (LV) endocardium. The impulses then proceed slowly from the endocardium to the epicardium throughout the right and left ventricles.^14–16

Electrocardiogram Waveforms

The initial electrical wave of a cardiac cycle represents activation of the atria and is called the P wave (Figure 10-9). Since the sinus node is located in the right atrium, the first part of the P wave represents the activation of this chamber. The middle section of the P wave represents completion of right atrial activation and initiation of left atrial activation. The final section of the P wave represents completion of left atrial activation. The AV node is activated during the inscription of the P wave. The wave representing electrical recovery of the atria is usually obscured by the larger QRS complex, representing the activation of the ventricles. From ECG lead II oriented from the cardiac base to the apex, the P wave is entirely positive, and the QRS complex is predominately positive. Minor portions at the beginning and end of the QRS complex may appear as downward or negative waves. The QRS complex may normally appear as one (monophasic), two (diphasic), or three (triphasic) individual waveforms. By convention, a negative wave at the onset of the QRS complex is called a Q wave. The first positive wave is called the R wave, regardless of whether or not it is preceded by a Q wave. A negative deflection following an R wave is called an S wave. When a second positive deflection occurs, it is termed R′. A monophasic negative QRS complex should be termed a QS wave.

FIGURE 10-9 The visible waveforms represent activation of the atria (P wave), ventricles (Q, R, and S waves), and recovery of the ventricles (T and U waves). The timing of activation of the structures of the pacemaking and conduction system is also indicated. AV, Atrioventricular; SA, sinoatrial.

The wave in the cardiac cycle that represents recovery of the ventricles is called the T wave. Since recovery of the ventricular cells (repolarization) causes a current counter to that of depolarization, one might expect the T wave to be inverted in relation to the QRS complex. However, epicardial cells repolarize earlier than endocardial cells, thereby causing the wave of repolarization to spread in the direction opposite that of depolarization. This results in a T wave deflected in a direction similar to that of the QRS complex (Figure 10-10). The T wave is sometimes followed by another small upright wave (the source of which is uncertain) called the U wave.

FIGURE 10-10 A, The frontal-plane view of the right and left ventricles, along with schematic recordings from left ventricular myocardial cells, on the endocardial (1) and epicardial (2) surfaces. B, The long-axis body surface electrocardiogram waveforms. The numbers below the recordings refer to the time (in seconds) required for these sequential electrical events.

The time from the onset of the P wave to the onset of the QRS complex is called the P-R interval, regardless of whether the first wave in this complex is a Q wave or an R wave (Figure 10-11). This interval measures the time between the onsets of activation of the atrial myocardium and the ventricular myocardium. The designation PR segment refers to the time from the end of the P wave to the onset of the QRS complex. The QRS interval measures the time from the beginning to the end of ventricular activation. Since activation of the thicker left ventricle requires more time than that of the right ventricle, the terminal portion of the QRS complex represents only LV activation.

FIGURE 10-11 The magnified recording from the cardiac long-axis viewpoint is presented, with the principal electrocardiogram segments (PR and ST) and intervals (P-R, QRS, Q-T, and T-P) indicated.

The term ST segment refers to the interval between the end of ventricular activation and the beginning of ventricular recovery. This term is used regardless of whether the final wave of the QRS complex is an R wave or an S wave. The junction of the QRS complex and ST segment is called the J-point. The interval from the onset of ventricular activation to the end of ventricular recovery is called the Q-T interval. This term is used regardless of whether the QRS complex begins with a Q wave or an R wave.

At low heart rates in a healthy person, the PR, ST, and TP segments are at the same horizontal level and form the isoelectric line. This line is considered as the baseline for measuring the amplitudes of the various waveforms. The TP segment disappears at higher heart rates when the T wave merges with the following P wave.^17–19

Determining Left Versus Right Cardiac Electrical Activity

It is often important to determine if an abnormality originates from the left or the right atrium or ventricle of the heart. The optimal site for recording left versus right cardiac electrical activity is located where the extension of the short axis of the heart (perpendicular to the inter-atrial and interventricular septa) intersects with the precordial body surface (lead V1) (Figure 10-12).

FIGURE 10-12 Magnified view of recording from the cardiac short-axis viewpoint with the principal electrocardiogram segments and time intervals indicated for the long-axis view. Lead V1 is shown.

The initial part of the P wave representing right atrial activation appears positive in lead V1 because of the progression of electrical activity from the inter-atrial septum toward the right atrial lateral wall. The terminal part of the P wave representing left atrial activation appears negative because of progression from the inter-atrial septum toward the left atrial lateral wall. This activation sequence produces a diphasic P wave (Figure 10-13).

FIGURE 10-13 The electrocardiogram waveforms are reproduced with the alterations, indicated by dashed lines, that would typically result from enlargements of the right (A) and left (B) atrial chambers and the right (C) and left (D) ventricular chambers and from right-sided (E) and left-sided (F) intraventricular conduction delays.

The initial part of the QRS complex represents the progression of activation in the interventricular septum. This movement is predominately from left to right, producing a positive (R wave) deflection at this left-sided versus right-sided recording site. The mid-portion of the QRS complex represents the progression of electrical activation through the right ventricular (RV) myocardium and the LV myocardium. Since the posteriorly positioned left ventricle is much thicker, its activation predominates that of the anteriorly placed right ventricle, resulting in a deeply negative deflection (S wave). The final portion of the QRS complex represents the completion of activation of the left ventricle. This posteriorly directed excitation is represented by the completion of the S wave.

The left versus right recording site is the key ECG view for identifying enlargement of one of the four cardiac chambers and localizing the site of a delay in ventricular activation (Figures 10-13 and 10-14). Right atrial enlargement produces an abnormally prominent initial part of the P wave, and left atrial enlargement produces an abnormally prominent terminal part of the P wave. Right ventricular (RV) enlargement produces an abnormally prominent R wave, whereas LV enlargement produces an abnormally prominent S wave. A delay in the right bundle branch causes RV activation to occur after LV activation is completed, producing an R′ deflection. A delay in the left bundle branch markedly postpones LV activation, resulting in an abnormally prominently S wave (see Figure 10-13).

FIGURE 10-14 The normal P-to-QRS relationship and appearances (A) are contrasted with various conditions that produce obvious abnormalities (B through D). Each example begins and ends during a T wave.

P-R Interval

The P-R interval measures the time required for the impulse to travel from the atrial myocardium adjacent to the sinus node to the ventricular myocardium adjacent to the fibers of the Purkinje network. This normally lasts 0.10 to 0.22 seconds. A major portion of the P-R interval is caused by the slow conduction through the AV node, and this is controlled by the sympathetic-parasympathetic balance of the autonomic nervous system. Therefore, the P-R interval varies with the heart rate, being shorter at faster rates when the sympathetic component predominates, and vice versa. The P-R interval tends to increase with age.²⁰

An abnormal P-wave direction is often accompanied by an abnormally short P-R interval, since the site of impulse formation has moved from the sinus node to a position closer to the AV node (Figure 10-15). However, a short P-R interval in the presence of a normal P-wave axis suggests either an abnormally rapid conduction pathway within the AV node or the presence of an abnormal bundle of cardiac muscle (bundle of Kent) connecting atria and ventricles and bypassing the AV node. This earlier-than-normal activation of the ventricular myocardium (ventricular pre-excitation) creates the potential for electrical reactivation or re-entry into the atria to produce a tachyarrhythmia (the Wolff-Parkinson-White [WPW] syndrome).

FIGURE 10-15 The normal P-to-QRS relationship (A) is contrasted with various abnormal relationships (B through F). Each example begins with the completion of a T wave and ends with the initiation of the T wave of the following cardiac cycle. The vertical time lines are at 0.2-second intervals. The P-R interval in (A) is therefore 0.2 seconds, which is near the upper limit of normal.

A longer than normal P-R interval in the presence of a normal P-wave axis indicates delay in impulse transmission at some point along the pathway between the atrial myocardium and the ventricular myocardium (Figure 10-15). When a prolonged P-R interval is accompanied by an abnormal P-wave direction, the possibility that the P wave is actually associated with the preceding rather than the following QRS complex should be considered. When such retrograde activation from ventricles to atria occurs, the P-R interval is usually even longer than the preceding QRS to P (R-P) interval. When the P-R interval cannot be determined because of the absence of any visible P wave, an obvious abnormality of the cardiac rhythm is present.

QRS Complex

The QRS complex is composed of higher-frequency signals than are the P and T waves, which causes its contour to be peaked rather than rounded. Positive and negative components of P and T waves are simply termed positive and negative deflections, whereas those of the QRS complex are assigned specific labels such as Q waves.

Q Waves

In some leads—V1, V2, and V3—the presence of a Q wave should be considered abnormal, and in all other leads (except III and aVR), a “normal” Q wave would be very small. The “upper limit of normal” for such Q waves in each lead is indicated in Table 10-1.²¹ The absence of small Q waves in leads V5 and V6 should be considered abnormal. A Q wave of any size is normal in III and aVR because of their rightward orientations. Q waves may be enlarged by conditions such as local loss of myocardium (infarction), hypertrophy or dilation of the ventricular myocardium, or abnormalities of ventricular conduction.

Table 10-1 Wave Duration Limits

R Waves

Since the precordial leads provide a panoramic view of the cardiac electrical activity progressing from the thinner right ventricle across the thicker left ventricle, the positive R wave normally increases in amplitude and duration from V1 to V4 or V5 (Figure 10-16). Reversal of this sequence with larger R waves in V1 and V2 can be produced by RV enlargement, and accentuation of the normal sequence with larger R waves in V5 and V6 can be produced by LV enlargement. Loss of normal R-wave progression from V1 to V5 may indicate loss of myocardium in the LV wall caused by myocardial infarction (MI).

FIGURE 10-16

The typical panoramic display of the six precordial leads of the electrocardiogram, illustrating the normal progression and regression of R-wave and S-wave amplitudes.

QRS Axis Determination

With the typical ECG display, a three-step method is used for determining the frontal plane QRS direction (termed axis):

FIGURE 10-17 Top left, The frontal-plane hexaxial reference system. Top right,The sectors indicating the various designations of the frontal plane QRS axis in the adults: normal axis (NA), right-axis deviation (RAD), left-axis deviation (LAD), and extreme axis deviation (EAD). Bottom, Examples of various frontal plane QRS axes: A, +60 degrees; B, +150 degrees; C, −30 degrees; D, −60 degrees; E, −120 degrees.

The frontal plane axis is normally directed leftward and either slightly superiorly or inferiorly: between –30 degrees and +90 degrees (see Figure 10-17). Therefore, the QRS complex is normally predominately positive in both leads I (with its positive pole at 0 degrees) and II (with its positive pole at +60 degrees). If the QRS is positive in lead I but negative in II, the axis is deviated leftward between –30 and –120 degrees. However, if the QRS is negative in I but positive in II, the axis is deviated rightward between +90 and +180 degrees. The axis is rarely directed entirely opposite the normal with predominately negative QRS orientation in both leads I and II.

The frontal plane axis is typically rounded to the nearest multiple of 15 degrees. If it is directly aligned with one of the limb leads, the axis is designated as –30 degrees, 0 degrees, +30 degrees, +60 degrees, and so on. If it is located midway between two of the limb leads, it is designated as –15 degrees, +15 degrees, +45 degrees, +75 degrees, and so on. Examples of patients with various frontal plane QRS axes are presented in Figure 10-17.

The normal frontal plane QRS axis is rightward in the neonate, moves to a vertical position during childhood, and then moves to a more horizontal position during adulthood. In normal adults, the electrical axis is almost parallel to the anatomic base to the apex axis of the heart, in the direction of lead II. However, the axis is more vertical in thin individuals and more horizontal in heavy individuals. A QRS axis more positive than +90 degrees in an adult should be designated right-axis deviation (RAD) (see Figure 10-17, B), and an axis more negative than –30 degrees at any age should be designated left-axis deviation (LAD) (see Figure 10-17, C). RV hypertrophy may produce RAD and LV hypertrophy LAD. An axis between −90 and +180 degrees should be considered extreme axis deviation (EAD) without designating it as either rightward or leftward (see Figure 10-17, E).

ST-Segment Morphology

The ST segment represents the period when the ventricular myocardium remains in an activated or depolarized state. At its junction with the QRS (J-point), it typically forms a nearly 90-degree angle and then proceeds horizontally until it curves gently into the T wave. The length of the ST segment is influenced by factors that alter the duration of ventricular activation. Points along the ST segment are designated with reference to the number of milliseconds beyond the J point, such as “J + 20,” “J + 40,” and “J + 60.”

The first section of the ST segment is normally located at the same horizontal level as the baseline formed by the PR segment and the TP segment, which fills in the space between electrical cardiac cycles. Slight up-sloping, down-sloping, or horizontal depression of the ST segment may occur as a normal variant. Another normal variant appears with early repolarization in the epicardial areas within the ventricles.²² This causes displacement of the ST segment in the direction of the following T wave. Occasionally, as much as a 4-mm ST elevation may occur in leads V1 to V3 in normal young males.²³ The appearance of the ST segment may also be altered during exercise or with an altered sequence of activation of the ventricular myocardium.

T-Wave Morphology

The smooth, rounded shape of the T wave resembles the shape of the P wave. However, variation of monophasic versus diphasic appearance in the various leads is normal. The initial deflection of the T wave is typically longer than the terminal deflection, producing a slightly asymmetrical shape. Slight “peaking” of the T wave may occur as a normal variant, and notching of the T waves is common in children. The duration of the T wave itself is not usually measured but is, instead, included in the Q-T interval, as discussed later. The amplitude of the T wave, like that of the QRS complex, has wide normal limits. It tends to diminish with age and is larger in males than in females. T-wave amplitude tends to vary with QRS amplitude and should always be greater than that of any U wave that is present. T waves do not normally exceed 5 mm in any limb lead or 10 mm in any precordial lead. The T-wave amplitude tends to be lower in the leads providing the extreme views of both frontal and transverse planes: T waves do not normally exceed 3 mm in leads aVL and III, or 5 mm in leads V1 and V6.²⁴

The direction of the T wave should be evaluated in relation to that of the QRS complex (Figure 10-18). The rationale for similar directions of these waveforms that represent the opposite myocardial events of activation and recovery has been presented earlier in the chapter (see “Basic Principles”). The method presented earlier for determining the direction of the QRS complex in the frontal plane should be applied for determining the direction of the T wave. The term QRS-T angle is used to indicate the number of degrees between the QRS complex and T-wave axes in the frontal plane.²⁵ A similar method can be applied in the transverse plane.

FIGURE 10-18 The normal QRS-to-T relationship (A) is contrasted with various abnormalities that may be associated with cardiac arrhythmias (B through E). Each example begins with the completion of a TP segment and ends with the initiation of the following TP segment.

Stay updated, free articles. Join our Telegram channel

Join