William E. DeTurk & Lawrence P. Cahalin
INTRODUCTION
The electrocardiogram (ECG) is a graphic representation of the depolarization of the heart. The physiology of depolarization of the heart is described in Chapter 5, and the particular pathways for conduction of the wave of depolarization are shown in Fig. 11-3. The ECG has undergone tremendous development and use since it was first applied to humans in 1887 by Augustus D. Waller.1 A brief history of the ECG is presented in Table 11-1.1–6
TABLE 11-1 History of the Electrocardiogram
Myocardial contraction (systole) and relaxation (diastole) are caused by myocardial cell depolarization and repolarization, respectively. The vector, or sum total, of all the electrical forces during any given cardiac cycle is called a wave of depolarization. This wave of depolarization moves down the normal conduction pathway from the atria to the ventricles, causes myocardial contraction, and produces deflections of the ECG waveform. Three of the most important concepts regarding interpretation of the ECG are that (1) as the wave of depolarization moves toward a positive electrode, a positive deflection is observed on the ECG; (2) as the wave of depolarization moves away from a positive electrode, a negative deflection is observed on the ECG; and (3) as the wave of depolarization moves perpendicular to a positive electrode, an isoelectric deflection is observed on the ECG (ie, a deflection with both positive and negative components). The ECG electrode and wires that attach to the electrodes transmit the heart’s electrical activity to an ECG recorder or display and are shown in Fig. 11-1. The ECG electrode is very simple in construction, yet yields much important information about the cardiovascular system. For the correct interpretation of single-and multiple-lead ECGs, it is essential to remember the three rules listed previously.
FIGURE 11-1 ECG electrodes consisting of a foam pad with an aggressive adhesive, a highly conductive electrolyte medium of silver–silver chloride, nipple clip onto which the wires attach, and the wires relaying the electrical activity of the heart to an ECG recorder or display.
Single-lead ECGs, or rhythm strips, are the graphic depiction of cardiac electrical activity from one particular view of the heart using two to three electrodes. Multiple-lead ECGs are the graphic depiction of cardiac electrical activity from multiple views of the heart using many electrodes. Multiple views are typically 12 in number and are grouped as limb leads and precordial leads. The standardized electrode placement for a typical 12-lead ECG recording is shown in Fig. 11-2.
FIGURE 11-2 Placement of ECG electrodes on the limbs (for limb leads) and across the chest (for precordial leads).
The pathway for the conduction of the wave of depolarization initiated by the sinoatrial (SA) node is shown in Fig. 11-3. This pathway includes the intranodal pathways, atrioventricular (AV) node, AV bundle of His, right and left bundle branches, and Purkinje fibers, from which the final wave of depolarization spreads across the ventricles in an inferolateral direction. Normally, the SA node initiates the wave of depolarization. However, it is important to note that, under certain conditions, other areas along the conduction pathway are capable of initiating an action potential and causing a wave of depolarization. The following sections will describe (1) the basic construct of the ECG, (2) skills required for ECG interpretation, (3) common ECG rhythm disturbances and methods to interpret them, (4) 12-lead ECG interpretation, and (5) cardiac pacemakers.
FIGURE 11-3 Conduction pathway that the wave of depolarization takes to elicit first atrial depolarization and subsequent contraction, and then ventricular depolarization and subsequent contraction. (Reproduced with permission from McPhee SJ. Pathophysiology of Disease: An Introduction to Clinical Medicine. 6th ed. New York: McGraw-Hill; 2010:250. Redrawn with permission from Ganong WF. Review of Medical Physiology. 22nd ed. McGraw-Hill; 2005.)
BASIC CONSTRUCT OF THE ELECTROCARDIOGRAM
An electrocardiograph machine is an ECG recording unit consisting of a signal amplifier, filter, writing unit, and paper printout unit. A motor pulls special heat-sensitive paper across a set of heated styluses, which “burn” a series of ECG complexes onto the paper. The paper has a grid printed on the surface, consisting of small and large boxes. The small boxes are 1.0 mm square; five small boxes form one large box (see Fig. 11-5A).
FIGURE 11-4 The typical ECG basic construct of the ECG with P, Q, R, S, T, and U waves; time intervals for the PR, QRS, and QT intervals; and ST segment. (Reproduced with permission from Tintinalli JE. Emergency Medicine: A Comprehensive Study Guide. 6th ed. New York: McGraw-Hill; 2004:181.)
FIGURE 11-5 Three methods of measuring the heart rate from an ECG. Note the small boxes (1 mm square) and large boxes (5 mm square) that form a grid. (A) Use of a heart rate ruler and 3-second marks to form a 6-second strip. Note that the reference arrow is aligned with the beginning of the R wave. The heart rate is measured at 84 complexes per minute. Use of the two 3-second marks (arrows), counting the number of complexes between these marks and extrapolating the results yields approximately the same value. (B) The counting mnemonic. (C) Use of the mnemonic to measure the heart rate. Note that the value of each little box between 50 and 60 is 2. Thus, counting backward from “50”to the R wave yields an approximate heart rate of 56 complexes per minute. ((C) Reprinted with permission from Dubin D. Rapid Interpretation of ECGs. 5th ed. Tampa, FL: Cover Publishing Company; 1996.)
The X axis, or horizontal axis, is time. The paper moves under the styli at a precise standardized speed, typically 25 mm/s. This dictates the value of one little box as 0.04 seconds, or 40 milliseconds. Similarly, the value of one big box is 0.20 seconds, or 200 milliseconds. There are five big boxes in 1 second. Many brands of ECG paper have marks placed on the top of the grid at 3-second intervals. As you will see, these marks can be used to measure heart rate (HR).
The Y axis, or vertical axis, is voltage. The amount of electricity generated by myocardial cells is quite small and is measured in millivolts. The height of any given waveform is a function of the amount of muscle mass it represents. Thus, voltage from atrial depolarization is quite small relative to the voltage generated by the larger ventricles and produces a small deflection of the waveform.
Correct ECG interpretation assumes that the machine is calibrated and is running in a standardized mode. Calibration marks should be included in any given ECG tracing. These marks provide a known voltage for a known period of time. When present, they will appear on the ECG paper as either a boxlike upward, horizontal, and downward deflection or a vertical spike that separates one group of leads from the other (see Fig. 11-26). An ECG machine that is calibrated to a standard moves ECG paper at 25 mm/s; a 1.0 mV signal deflects the stylus by 10 mm (10 mm/mV).
DEPOLARIZATION OF THE HEART
Atrial Depolarization
Depolarization of the atria normally begins at the SA node. The SA node consists of a bundle of specialized neural conduction fibers, which spontaneously depolarizes and generates an action potential as ions move from one area to another. Once a critical concentration of sodium ions moves into the sarcoplasmic reticulum of the SA node, threshold is reached and an action potential is released. A wave of depolarization spreads downward to the AV node, bundle of His, bundle branches, and Purkinje fibers. This propagation of electrical activity can be captured with ECG electrodes and recorded on ECG recording paper with the equipment shown in Figs. 11-1 and 11-2. The typical ECG waveform representing one wave of depolarization (or one cardiac cycle) is shown in Fig. 11-4. The P wave represents atrial depolarization. Several specific aspects of the SA node give the P wave and PR interval their characteristic appearance. These aspects include the location, ion concentrations, and inherent atrial pathways down which the SA node action potential propagates.8,9 The P wave is the result of sodium and calcium ion influx that produces atrial depolarization and contraction.
Atrioventricular Depolarization
Like the SA node, the AV node is also composed of a bundle of specialized neural conduction fibers, but they differ in construction from those of the SA node and therefore yield a different shaped action potential (Fig. 11-3). The PR segment represents conduction from the AV node through the bundle of His. Conduction velocity through AV node fibers is slower than that of the SA node. This contributes to the flat piece of baseline that separates the P wave from the QRS complex. The slow conduction velocity, which is due to differing ion concentrations and myocardial tissues, decreases the rapidness of the upslope for action potential development and slightly increases the time for repolarization, as fewer potassium ions move into the sarcoplasmic reticulum of the AV node.8,9 This slowing of conduction through the AV node allows time for the atria to contract, and “top off” blood in the ventricles, which will in turn provide a “quick stretch” to the ventricles and enhance ventricular contraction.
Ventricular Depolarization
The ventricles of the heart propagate an action potential that is, again, different in appearance from SA and AV node action potentials. The QRS complex represents ventricular muscle depolarization. This waveform is typically wide, reflecting depolarization of nonspecialized, slow-conducting myocardium, and tall, reflecting the large amount of muscle mass present in the ventricles and the large voltage that such muscle mass generates. The morphology of the QRS complex is primarily due to ion concentrations within ventricular myocardium, which decrease the rapidness of the upslope for action potential development and increase the time for repolarization. Both of these aspects produce a wider and taller waveform.8,9 The Q wave is the result of an influx of sodium and calcium ions into ventricular muscle (producing the negative deflection) that initiates ventricular contraction. The R and S waves are the result of greater levels of ion exchange in ventricular muscle during ventricular contraction.
The ST segment represents early ventricular repolarization. The T wave represents later ventricular repolarization. These waveforms are the result of an increase in potassium ion concentration within the sarcoplasmic reticulum of the myocardial fibrils and produce diastolic depolarization (needed for myocardial relaxation). The U wave is only occasionally seen on ECG and is the result of abnormal electrolyte and ion concentrations (either depleted or excessive concentrations).8,9 Each of these waveforms represents areas that are very important for myocardial performance and will be discussed in greater detail in the following sections.9–12
ELECTROCARDIOGRAPHIC INTERPRETATION—BASIC SKILLS NEEDED
The basic skills needed for ECG interpretation include determination of (1) heart rate and rhythm for the recognition of rhythm disturbances, (2) relationships among the different waves of an ECG complex and the rhythm for the recognition of some rhythm disturbances, and (3) presence of myocardial ischemia, because most disturbances in cardiac rhythm are due to myocardial irritability from myocardial ischemia.9–12 The following sections will review each of these essential skills.
Determining the Heart Rate
The heart rate can be measured using the methods already presented in Chapter 10. These include arterial palpation, cardiac auscultation, and use of a heart rate digital display watch. The ECG is considered the gold standard for determination of heart rate and as such is a good reference to measure the accuracy of these other heart rate measurements and to identify location of the cardiac cycle for these other examination techniques.9–12 Measuring the heart rate from an ECG tracing can be performed using a heart rate ruler, estimating the heart rate using the 6-second marks on the ECG recording paper, or using a counting mnemonic representative of the mathematical calculations used to measure heart rate. The heart rate ruler method is simplest, whereas the counting mnemonic becomes less accurate at high and low heart rates.
Heart Rate Ruler Method
Measurement of the heart rate with a heart rate ruler simply requires one to place the reference point of a heart rate ruler on one of the waves of an ECG complex (often the R wave because it is large and observable) and identify the point where the same wave of a subsequent ECG complex falls (either two or three ECG complexes to the right of the original ECG complex, see Fig. 11-5A). This method quickly and accurately measures the number of beats per minute by measuring the number of cardiac cycles (ECG complexes) that fall between the reference point and heart rate reference points that have been plotted on the heart rate ruler based on mathematical calculations. It is important to note that the use of the heart rate ruler presupposes a regular rhythm. Inaccuracies result if the interval between complexes changes from beat to beat.9–12 If such is the case, use of the 6-second mark will yield more accurate results.
Six-Second Mark Method
Measurement of the heart rate using the 6-second marks on ECG recording paper can also be done quickly but may be less accurate in determining the true heart rate. The method simply involves counting the number of ECG complexes between two 3-second marks on the ECG paper and multiplying this number by 10, which yields the number of ECG complexes in 60 seconds (or the number of cardiac cycles/min) (see Fig. 11-5A). Inaccurate heart rates may be measured if the number of ECG complexes between the 6-second markers is incorrectly counted or if over the course of a minute the rhythm changes. However, the measurement of heart rate in an ECG with frequent rhythm disturbances is best accomplished using the 6-second mark method. Rhythm disturbances that would be appropriate for this method of heart rate measurement include atrial fibrillation (afib) and occasional to frequent premature atrial or ventricular contractions.9–12 It should be noted that slight inaccuracies in one 6-second strip become magnified by 10 when the heart rate is expressed in beats per minute. Therefore, multiple 6-second strips yield more accurate results.
Counting Mnemonic Method
The measurement of heart rate via counting mnemonic can also be used by applying the mnemonic scale shown in Fig. 11-5B. This counting mnemonic is based on the same mathematical calculations that allow the heart rate to be measured using the heart rate ruler. The mnemonic is very simple and requires that the student memorize the numeric sequence “300-150-100-75-60-50.” These numbers represent the heart rates obtained when the next consecutive waveform falls on a heavy black line, that is, the edge of a large box. Note that the difference between 300 and 150 is 150; the “value” of each of the five little boxes between 300 and 150 is 30. Similarly, the difference between 75 and 60 is 15; the “value” of each little box is 3. The “value” of each little box changes as a function of your location in the mnemonic.
This information is useful when the next consecutive complex fails to fall on a heavy black line and will “fine-tune” your heart rate. The application of the counting mnemonic is as follows:
1.Identify a waveform of the ECG complex that falls on or near the heavy black line of a large box. Often the R wave is used because it is large and identifiable, but it need not be so—Q waves and S waves are also acceptable.
2.Identify the same wave in the next consecutive ECG complex (the next complex to the right of the first complex).
3.Apply the counting mnemonic by counting cycles across the big boxes until the next consecutive waveform is crossed; then stop counting.
4.The point where the same wave of the second consecutive complex falls (often near a large box) in the counting mnemonic yields the approximate heart rate in beats per minute.
5.Count backward (to the left) from the heavy black line of the large box just to the right of the second consecutive waveform using the value of each little box until you land on the second waveform. This final number represents the most accurate estimation of heart rate.9–12 See Fig. 11-5C for an example of the application of the counting mnemonic method.
Determining the Heart Rhythm
Determining the rhythm of the heart is critically important when attempting to interpret different types of rhythm disturbances. Determination of the rhythm of the heart simply involves evaluating the regularity of the heart’s discharge of electrical activity (or ECG complexes), which can be accomplished via palpation of the arterial pulse (see Chapter 10), observation of the regularity of the ECG complex on an ECG screen (which can also be heard with a “beep” when the ECG complex appears on the screen), or actual measurement on a recorded ECG. The rhythm of the heart can be measured on a recorded ECG using one of the three different methods, including a quick glance at the regularity between ECG complexes, use of a caliper, and use of marks on paper.9–12 Heart rhythm is expressed as either “regular” or “irregular.” Sometimes an irregular rhythm has a recurring pattern within it; for example, every third impulse is missing. These rhythms are then expressed as “regularly irregular.” This will be discussed in greater detail later in this chapter.
Quick Glance of the Regularity Between ECG Complexes
As mentioned earlier, a quick glance at an ECG screen or a recorded ECG can provide important information about the regularity between ECG complexes and whether or not a rhythm disturbance exists. Almost all rhythm disturbances display (or audibly “beep”) irregularity between ECG complexes. The time period between ECG complexes is unpredictable and not consistently equal. An example of a cardiac rhythm irregularity can be seen in Fig. 11-6.
FIGURE 11-6 Use of calipers to assess heart rhythm. Note that once the R-R interval is obtained the calipers are simply “marched out” across the tops of the remaining R waves. This ECG reflects a grossly irregular rhythm. (Used with permission from J. Huff, ECG Workout: Exercises in Arrhythmia Interpretation, 3rd ed., Lippincott Williams & Wilkins, 1997.)
Use of a Caliper
A cardiac caliper is similar to the long legs of a compass and can be positioned on the same waves of two consecutive ECG complexes (see Fig. 11-6). Some cardiac calipers allow for the measured distance between waves to be locked into the measured distance (by turning a small set screw at the end of the caliper that keeps the legs of the caliper from moving). This locked position represents the distance between two consecutive ECG complexes. This interval can then be used to plot the distance between remaining ECG complexes, termed marching out the rhythm.9–12 Perfect alignment of ECG complexes with the points of the caliper across the rhythm strip signifies a regular rhythm. The inability to march out successive ECG complexes signifies an irregular rhythm.9–12
Use of Marks on Paper
A “crude” method that can be used to examine regularity between ECG complexes involves identifying a specific wave in one ECG complex (again, often the R wave is chosen because it is largest and easily identified), marking its location on a piece of paper, and then identifying the same wave in the next consecutive ECG complex and marking its location on the same piece of paper. These two marks are then marched out between the next two consecutive ECG complexes, and the marks are examined for alignment within the two consecutive ECG complexes. Examining the alignment of the marks on paper with pairs of ECG complexes is continued until all pairs of ECG complexes have been measured. If the heart rhythm is regular, the marks on the paper will line up in perfect alignment with each subsequent pair of ECG complexes. If, however, the rhythm is irregular, the marks on paper would not line up; for example, they would be lined up with the first ECG complex and not the second (because of irregularity between the complexes).
Determining the Relationships Among the Different Waves of an ECG Complex and the Rhythm
Determining the relationships of different waveforms within and between ECG complexes in view of the heart rhythm is helpful in identifying some disturbances in cardiac rhythm. The position of the waves on an ECG tracing should always follow the sequence presented in Fig. 11-4. The P wave should be first, followed by the QRS complex, T, and U waves (if present). When this order is not observed, it is very likely that a cardiac rhythm disturbance exists.9–12 Of equal importance are the intervals between these waves. Each of these waves has a specified interval of time between it and the next wave (Fig. 11-4). If the intervals between one or more of these waves is not within normal limits or if it is irregular (changing from one ECG complex to another), it is also very likely that a cardiac rhythm disturbance exists.9–12 For example, the normal specified time interval between the P wave and the R wave (PR interval) should be no greater than 0.20 seconds (or one big box). If the time interval between these two waves is greater than 0.20, a cardiac rhythm disturbance exists. Likewise, if the time interval between these two waves changes from one ECG complex to another, then another type of cardiac rhythm disturbance exists. Examples of specific rhythm disturbances will be presented immediately after the next section. The next section will provide a brief overview of methods to recognize the primary cause of cardiac rhythm disturbances and that of myocardial ischemia.
Determining the Presence of Myocardial Ischemia
Myocardial ischemia is the most common cause of cardiac rhythm disturbances.9–12 It can be observed on ECG by examining the position of the ST segment of the ECG (Fig. 11-4). Myocardial ischemia typically produces ST-segment depression, which can be measured with a ruler or any straight-edged device. The process is as follows:
1.The PR intervals of two successive complexes are identified. A ruler is placed horizontally from one PR interval to the next PR interval. This horizontal line from two successive PR intervals can be marked with a pencil and identifies the isoelectric line (the line of equal charge or the midpoint of depolarization and repolarization).
2.The J point of the complex to be evaluated is identified. The J point is defined as the break point between the end of the QRS complex and the beginning of the ST segment.
3.The examiner moves to the right, away from the J point 2 little boxes, or 0.08 seconds.
4.It is at this point that the magnitude of ST segment depression is measured by counting the number of boxes vertically from the point of the ST segment, that is, two little boxes to the right of the J point to the isoelectric line.
5.A measured value of depression of the ST segment that is greater than 1.0 mm is highly suggestive of myocardial ischemia.
See Chapter 12 for an additional description, figures, and examples of ST-segment measurement.
CLINICAL CORRELATE
It is important that physical therapists develop assessment skills for the presence of myocardial ischemia through accurate measurement of ST-segment changes. These changes typically come on with exercise and go away with rest, as the demand for oxygen by the myocardium outstrips the supply. These ECG changes are usually, but not always, accompanied by complaints of chest pressure. Once evidence of myocardial ischemia is obtained, exercise should be terminated.
It should be noted that the morphology, or shape, of the ST segment also contributes to the diagnosis of ischemia. Downsloping or horizontal ST segments are more diagnostic than ST segments that are upsloping. Fig. 11-16demonstrates downsloping ST-segment depression. Additionally, a number of other things may cause ST-segment depression and are listed in Box 11-1. The presence of one or more of the items listed in Box 11-1 may decrease the likelihood that ST-segment depression is due to myocardial ischemia. See Chapter 12 for further discussion of ST-segment interpretation and the clinical application of these data.
BOX 11-1
Causes of ST-Segment Depression or Elevation
1.Myocardial ischemia or infarction
2.Coronary artery spasm
3.Electrolyte abnormalities
4.Left ventricular hypertrophy
5.Interventricular conduction delays (eg, bundle branch blocks)
6.Atrial fibrillation or flutter
7.Digoxin
8.Pacemaker
Myocardial ischemia due to coronary artery spasm may present with ST-segment elevation. The method to measure ST-segment elevation is similar to the measurement of ST-segment depression, only measuring from the isoelectric line to the top of the elevated ST segment, 0.08 seconds to the right of the J point. Finally, ST-segment elevation is also associated with acute myocardial infarction, which will be discussed later in this chapter.
DISTURBANCES IN CARDIAC RHYTHM
Whereas heart rate is quantified as beats per minute, heart rhythm is qualified as either regular or irregular. Regular rhythms, like music, are predictable in nature—we know when the next beat will fall. Irregular rhythms are either irregularly irregular (completely random) or regularly irregular—there is a pattern to the irregularity.9–14
Heart rhythm may be assessed through cardiac auscultation or through peripheral pulse palpation. Indeed, palpation of peripheral pulses is frequently where rhythm disturbances are first discovered. Detection of arrhythmias through peripheral pulse palpation presumes a normal vascular system.
CLINICAL CORRELATE
Advanced atherosclerosis, which occludes the brachial artery, can preclude accurate assessment of rhythm. This should prompt the physical therapist to an assessment of rhythm through cardiac auscultation.9–14
Alterations in rhythm may originate from within the normal conduction pathway, specifically, from normal pacemakers of cardiac depolarization: the SA node or the AV node. These normal pacemakers possess their own intrinsic firing rates. The normal rate of spontaneous depolarization of the SA node is between 60 and 100 bpm. The normal rate of the AV node is between 40 and 60 bpm. If, for whatever reason, the AV node becomes dysfunctional and fails to fire, even the ventricles can assume pacemaker control, at their own inherent rate of 20 to 40 bpm. As we shall see, the pacemaker with the highest rate of discharge assumes pacemaker control of the heart.
This principle of the highest-order pacemaker acts as a safety net, which turns on as a progressive fallback system when human viability is threatened.9–14
Rhythm disturbances may also arise from outside the normal conduction pathway. These ectopic foci consist of areas of irritable myocardium, which can spontaneously depolarize. This wave of depolarization spreads outward and in the process, depolarizes the normal conduction pathway.
Rhythm disturbances can arise from the atria, from the junctional (AV nodal) area or from the ventricles. This section will describe commonly encountered arrhythmias in order from the top, at the level of the atria, and down to the bottom, at the level of the ventricles.9–14
Sinus Node Rhythm Disturbances
In a healthy normal subject at rest, the sinoatrial node (SA node) spontaneously depolarizes at a rate between 60 and 100 bpm. This positive wave of depolarization proceeds down the normal conduction pathway, depolarizing first the atria, then the ventricles. The rhythm is regular; that is, the distance between R and R intervals is fixed. Assuming normal excitation–contraction coupling, ventricular depolarization causes ventricular contraction. Ventricular contraction expels a bolus of blood from the chamber of the left ventricle, such bolus traveling down the arterial tree and giving rise to a peripheral pulse that can be palpated at any of the several sites where the artery travels close to the skin surface. The term normal sinus rhythm (NSR) implies both a heart rate between 60 and 100 bpm and a spontaneous depolarization initiated by the SA node9–14 (see Fig. 11-7).
FIGURE 11-7 Normal sinus rhythm, rate 86 bpm.
A sinus rate may exceed 100 bpm and is termed sinus tachycardia (ST) (see Fig. 11-8). Sinus tachycardia may pose a threat to the patient, depending on the rate. Rapid ST narrows diastolic filling time and reduces stroke volume; this in turn may reduce cardiac output and cause the patient to become dizzy or even lose consciousness. Although rare, sinus tachycardia may come on suddenly and have a sudden termination. This is termed paroxysmal atrial tachycardia (PAT), and is sometimes associated with digitalis toxicity (see Fig. 11-9). Patients may experience palpitations, accompanied by feelings of light-headedness or even syncope. Many patients respond favorably to carotid sinus massage. This maneuver involves direct massage of the area over the bifurcation of the carotid artery in an effort to enhance parasympathetic nervous system activity and “break” this rapid, runaway rate.9–14
FIGURE 11-8 Sinus tachycardia, rate 120 bpm.
FIGURE 11-9 Paroxysmal atrial tachycardia (PAT), rate 167 bpm of the PAT. Note the sudden onset and termination.
Sinus tachycardia is normal during exercise, as the demand for blood and oxygen by working skeletal muscle is normally met by increases in both heart rate (HR) and stroke volume.
A sinus rate may fall below 60 bpm and is thus termed sinus bradycardia (SB) (see Fig. 11-10). Sinus bradycardia may also pose a danger to the patient, particularly if the HR is very low. This time the reduction in cardiac output is due to diminished HR, which also cause dizziness and syncope. Sinus bradycardia is normal in athletes where SB is compensated by enhanced stroke volume, which is due to an exercise-induced increase in left ventricular muscle mass and better contractility.9–14
FIGURE 11-10 Sinus bradycardia, rate 54 bpm.
Yet another sinus node disturbance in rhythm is caused by changes in intrathoracic pressure and is termed sinus arrhythmia or respiratory arrhythmia. Alterations between inspiration and expiration produce phasic increases and decreases in intrathoracic pressure that impacts on venous return and thus heart rate. Sinus arrhythmia is better thought of as a normal heart rhythm variant. Many healthy individuals demonstrate sinus arrhythmia on routine ECG, and it rarely has any clinical relevance because there is no hemodynamic compromise9–14 (see Fig. 11-11).
FIGURE 11-11 Sinus arrhythmia, rate 60 bpm. Note the gradual shortening and prolongation of the R-R interval, consistent with the respiratory cycle.
CLINICAL CORRELATE
The significance of normal sinus rhythm, sinus tachycardia, and sinus bradycardia resides within the context of additional data. Normal sinus rhythm at rest is a normal finding; NSR at a high level of exercise is abnormal. Similarly, sinus bradycardia in a patient with an acute MI is quite different from SB in a 24-year-old athlete. Physical therapists should avoid evaluating a single piece of data in isolation; rather, ECGs should be evaluated within the context of the total patient, and a clinical decision should be made on that basis.
Occasionally the SA node becomes lazy; the ECG demonstrates an abnormally long cycle between complexes. This phenomenon is called sinoatrial block, or, more commonly, sinus pause. Although it is difficult to determine the etiology, short sinus pauses are rarely problematic. Prolonged sinus pauses, however, can predispose to dizziness and syncope and require intervention, usually pacemaker implantation (see Fig. 11-12). A prolonged sinus pause should give rise to an escape beat or an escape rhythm. An escape beat may originate from the atrium, the AV node, or the ventricles. An escape beat responds to flat pieces of baseline that are void of electrical activity by spontaneously depolarizing the myocardium and is yet another safety net that is activated to help restore a normal rhythm and maintain cardiac output9–14 (see Fig. 11-12).
FIGURE 11-12 Sinus pause, following NSR at a rate of 60 bpm. Note the junctional escape beat, which reestablishes the rhythm.
Premature Atrial Contractions
Sinus tachycardia, SB, and sinus arrhythmia all originate from spontaneous depolarization of the SA node. However, in certain individuals and in some circumstances, a spontaneous wave of depolarization can originate from outside the normal conduction pathway. An ectopic focus (pleural, foci) is an area within the myocardium that, in certain circumstances, can spontaneously depolarize. When it does so, it “jumps ahead” of SA node depolarization and is thus premature. Indeed, prematurity is one of the hallmarks of a premature atrial contraction (PAC). PACs originate from areas of irritable, sometimes ischemic, myocardium that form the wall of the atrium. The P wave of a PAC may look different from the P wave of sinus node origin; this is because the P wave comes from a different place within the atrium. However, the atria are relatively small compared to the ventricles; thus, failure to detect a different looking P wave should not in and of itself eliminate the presence of a PAC. Because the SA node is briefly “silenced” as a pacemaker by the PAC, the SA node must reset itself in order to restore a new normal sinus rhythm. The reset of the SA node is another hallmark of a PAC. Once the AV node has been depolarized, the ventricular response to a PAC is usually normal. Therefore, most of the time, the QRS complex looks the same as a normal ECG complex9–14(see Fig. 11-13).
FIGURE 11-13 Normal sinus rhythm, rate 74 bpm, with one PAC. Note that the PAC resets the sinus node at a slower HR.
PACs are characterized as isolated if they occur as a single ECG event. They are classified as bigeminal if every other ECG event is a PAC. Trigeminy indicates that two ECG events are normal for every premature complex. Two PACs in a row are termed paired PACs or couplets. Occasional isolated PACs pose no threat to patients. There is no significant alteration in heart rate and thus no reduction in cardiac output.9–14
Atrial Flutter
A single irritable ectopic focus can fire occasionally and capture the ventricle, giving rise to a PAC. However, a single ectopic focus also can fire repetitively and so rapidly that the slow-conducting AV node fails to conduct every impulse. This arrhythmia gives rise to an ECG complex characterized by multiple P waves to every QRS response. In atrial flutter (aflutter), the P waves have a typical “saw-tooth” pattern (see Fig. 11-14). This shows four P waves for every QRS complex. In general, the rate of the flutter waves is between 200 and 300 bpm, and the P waves–QRS complex ratio is commonly 2:1. This ratio can change, however, sometimes to 3:1, which slows the ventricular response and decreases cardiac output. Atrial flutter is commonly found in patients with ischemic heart disease or with patients recovering from any acute illness; it may appear transiently after heart surgery.11 The variability in ventricular response makes atrial flutter somewhat unstable and requires treatment.9–14
FIGURE 11-14 Atrial flutter, with an atrial rate of 428 bpm and a rapid ventricular response of 110 bpm. Note the 4:1 AV conduction.
Atrial Fibrillation
Atrial flutter is characterized by repetitive firing of a single ectopic atrial focus, with periodic transmission of the depolarization wave through the AV node down to the ventricles. The P waves are well-formed and similar in morphology, implying that there is a high degree of organization in both atrial depolarization and atrial contraction. In atrial fibrillation (afib), this high degree of organization is lost. An afib is characterized by multiple ectopic foci, all firing at random throughout the cardiac cycle. There is no single, unified wave of depolarization in the atria and thus no organized myocardial contraction. Indeed, the atria have been characterized as “quivering like a bag of worms (anon).” The ventricular response is extremely variable; occasionally, enough voltage will summate to depolarize the AV node, which will then propagate the impulse down the His bundle to the ventricles and cause ventricular depolarization in the usual manner9–14 (see Fig. 11-15). Afib is characterized by an irregular, jagged baseline and an irregular ventricular response, and it can be identified by (1) a constantly changing R-to-R wave interval, (2) absence of a P wave, and (3) jagged (fibrillatory) baseline.
FIGURE 11-15 Atrial fibrillation, with an irregular ventricular response of 70 bpm. Note the absence of P waves and the jagged baseline.
Because the ventricular response is so variable, it is desirable to calculate the ventricular rate. This requires that the practitioner count the number of QRS complexes in a 6-second strip and multiply by 10. Heart rates in afib may be categorized and documented as
60 to 100 bpm = afib with moderate ventricular response (MVR),
> 100 bpm = afib with rapid ventricular response (RVR),
and
< 60 bpm = afib with slow ventricular response (SVR).
Afib is produced by a variety of disease processes, including rheumatic heart disease, ischemic heart disease, hypertensive heart disease, and heart failure.11 New-onset afib requires treatment, either by medications that slow conduction through the AV node by prolonging refractoriness (eg, digitalis, verapamil) or by electrical stimulation (eg, DC defibrillation). Chronic afib is well-tolerated by many patients. The “atrial kick” provided by an atrium contracting in syncytium tops off an already full ventricle and thus contributes only a small additional amount of blood to stroke volume. Additionally, the risk of conversion to NSR outweighs the benefits of such a procedure.9–14
Atrioventricular Node Rhythm Disturbances (Junctional Rhythms)
As mentioned previously, in circumstances where the SA node becomes electrically silent, the AV node can take over pacemaker function. The AV node can also spontaneously depolarize, giving rise to a junctional premature contraction (JPC). Because the AV node is part of the supraventricular conduction system, the QRS complex in a JPC appears normal, that is, is of normal width. The P wave is absent, which is consistent with the loss of SA node input from above9–14 (see Fig. 11-16).
FIGURE 11-16 Junctional rhythm, rate 50 bpm. Note the absence of P waves and the narrow, normal looking QRS complex. Note the presence of ST-segment depression.
The normal resting rate of depolarization of the AV node is 40 to 60 bpm. The AV node, however, does respond to exercise by increasing its rate, and physical therapists may be called on to develop an exercise prescription in patients with junctional rhythms to attain a training effect.
Junctional premature contractions are best thought of as an escape rhythm due to loss of the SA node, rather than to true arrhythmias. Causes of JPCs include those of suppression of SA node function, for example, myocardial ischemia and particularly right coronary artery lesions that supply the SA node. Treatment is directed toward treating the cause of default to a lower order pacemaker.9–14
Heart Blocks
Heart blocks occur when conduction from the SA node to the AV node gets altered. This alteration typically occurs at the level of the AV node and can present either as a delay in conduction or as a complete block. Heart blocks are graded by levels of severity from first degree, through second degree, to third degree.9–14
First-Degree Heart Block
Recall that the normal PR interval is short, that is, less than 0.20 seconds long. In first-degree AV block, conduction from the atria to the ventricles is delayed, causing prolongation of the PR interval (see Fig. 11-17). Note that while the PR interval is prolonged, conduction proceeds through the AV node and down the common bundle of His, and the ventricles are still captured. First-degree AV block is frequently benign and commonly occurs in endurance-trained athletes. These individuals also demonstrate a shift toward vagal tone, producing sinus bradycardia coupled with a slowing of conduction through the AV node.9–14
FIGURE 11-17 First-degree AV block, rate 48 bpm. Note the prolonged PR interval measuring 0.30 seconds.
Second-Degree Heart Block
There are two types of second-degree AV block. In Mobitz type I heart block there is gradual prolongation of the PR interval until a QRS complex is dropped. After the dropped QRS complex, the next beat recaptures the ventricles with a shortened PR interval, and then gradual prolongation of the PR interval repeats (see Fig. 11-18). Also known as Wenckebach phenomenon, the lesion is usually located within the AV node and is usually caused by an excess in parasympathetic output to the AV node or medications that cause parasympathetic effects. Wenckebach is usually innocuous and frequently occurs transiently in the setting of acute MI.9–14
FIGURE 11-18 Second-degree AV block, Mobitz type I; atrial rate 72 bpm, ventricular rate approximately 55 bpm. Note the gradual prolongation of the PR interval, until a QRS complex is dropped.
Second-degree AV block, Mobitz type II, is also characterized by dropped QRS complexes. However, the PR interval is fixed and remains unchanged throughout consecutive cardiac cycles9–14 (see Fig. 11-19).
FIGURE 11-19 Second-degree AV block, Mobitz type II; atrial rate 130 bpm, ventricular rate approximately 41 bpm. Note the fixed PR interval, with every third P wave capturing a QRS complex.
Both second-degree AV blocks are associated with rheumatic fever, acute inferior wall MI, and digitalis toxicity. They rarely progress to complete heart block (CHB).
Third-Degree Heart Block
A third-degree heart block is a complete heart block and is characterized by complete AV dissociation, with atrial and ventricular rhythms functioning independently9–14 (see Fig. 11-20). This figure shows a fixed P-to-P interval and a fixed R-to-R interval, with resultant variation in PR interval, confirming complete AV dissociation and complete heart block. CHB is frequently compensated for by an escape rhythm that originates at a site distal to the lesion. However, if these escape beats are not forthcoming, the patient could lose consciousness, or worse. Therefore, CHB usually requires the insertion of an artificial pacemaker.9–14
FIGURE 11-20 Third-degree AV block, atrial rate 88 bpm, ventricular rate approximately 38 bpm. Note the relatively fixed P–P interval, the fixed R–R interval, and the variable PR interval, indicating complete dissociation between the atria and ventricles.
Premature Ventricular Contractions and Ventricular Tachycardia
Many of the same issues that guided discussion of premature atrial contractions hold true for premature ventricular contractions (PVCs). The irritable ectopic focus described earlier now resides in the myocardium of the ventricle. This focus consists of irritable, usually ischemic, myocardium that spontaneously depolarizes and “jumps the gun” ahead of the wave of depolarization traveling down the normal conduction pathway from the atria. As in PACs, prematurity is also the hallmark of the PVC. However, the QRS complex of most PVCs is wide and bizarre looking. PVCs are wide because they travel through slower conducting myocardium; they are frequently tall because the muscle mass that they travel through generates more voltage than neural elements found in conduction tissue. PVCs do not reset the SA node; the atria are relatively “protected” from spontaneous depolarization originating from the ventricles by the common bundle of His. The maintenance of normal, undisturbed P wave activity across the PVC establishes complete AV dissociation at that point in time and is a hallmark of the PVC.9–14
PVCs take on added significance because their presence, in the setting of ischemic heart disease, places the patient at higher risk for reinfarction and sudden death. PVCs are also problematic because they can be hemodynamically compromising and can degenerate into a lethal arrhythmia. It is helpful, therefore, to describe PVC activity in terms of frequency, morphology, and relationship to the cardiac cycle.9–14
Like PACs, PVCs can be described as isolated, bigeminal, trigeminal, and paired. However, PVCs arise from the much larger muscle mass of the ventricles and thus may compromise stroke volume and cardiac output. For this reason, the frequency of PVC activity is important as well as their relative proximity to each other.
CLINICAL CORRELATE
Movement from ventricular trigeminy through ventricular bigeminy to PVC pairs increases PVC significance, especially in the setting of an acute MI or during exercise9–14 (see Fig. 11-21).
FIGURE 11-21 Unifocal PVCs, presenting as ventricular trigeminy. Note that the sinus node is not reset and continues to depolarize “on time” through the PVCs.
PVCs can arise from multiple foci within the ventricle. These are termed multifocal PVCs (see Fig. 11-22). This figure shows two bizarre, premature complexes that look different from each other. This is because they originate from different areas of the ventricles. Multifocal PVCs are more significant than unifocal PVCs because their activity can summate and produce more PVCs per minute.9–14
FIGURE 11-22 Multifocal PVCs, presenting as a PVC pair or couplet. The underlying sinus rate is 63 bpm. Note the P wave in the negative limb of the first PVC.
PVCs can also be evaluated on the basis of their relationship to the previous ECG cycle. Occasionally, a PVC is so premature that it appears on the T wave of the preceding ECG complex. This is called an R-on-T PVC (see Fig. 11-23). The presence of R-on-T PVCs is of particular concern because they depolarize the myocardium during its relative refractory period. This is a particularly vulnerable period in the repolarization phase and can set up a series of rapid sequential depolarizations termed ventricular tachycardia (vtach or VT).9–14 VT is defined as three or more PVCs in a row at a rate of > 100 bpm (see Fig. 11-24). Chapter 12 will describe the significance of PVC behavior as it relates to exercise.
FIGURE 11-23 R-on-T PVC. The underlying sinus rate is 105 bpm.
FIGURE 11-24 A self-limited burst of ventricular tachycardia. This should be documented by the clinician as five PVCs in a row at a rate of 210 bpm. Note the profound ST-segment depression, indicating myocardial ischemia that sets the stage for this dangerous arrhythmia.
Ventricular Fibrillation
Ventricular tachycardia can degenerate into a lethal arrhythmia known as ventricular fibrillation (vfib). Like afib, vfib is caused by multiple ectopic foci, all firing at random. There is no organization to the ECG waveform, and there is no organized wave of depolarization. The ventricles thus fail to contract in syncytium and instead “quiver like a bag of worms” (anon)9–14 (see Fig. 11-25).
FIGURE 11-25 Coarse ventricular fibrillation. Note the loss of electrical organization in the irregularly shaped waveforms that reflect multiple ventricular foci firing randomly in vfib. This lack of organization prevents measurement of heart rate.
Vtach can be restored to NSR through the use of synchronized cardioverters, machines that deliver a preselected amount of energy by way of paddles applied over the chest. These devices “read” the patient’s ECG waveform and time the delivery of countershock to the patient’s R wave. In this way, the practitioner avoids delivery of shock during the refractory period of myocardial repolarization and prevents the onset of vfib. Ventricular fibrillation, on the other hand, is corrected using a defibrillator device.9–14
CLINICAL CORRELATE
It should be noted that it is easier to bring patients back from vtach than it is from vfib. Physical therapists encountering a patient in sustained vtach should initiate emergency procedures by calling a code. This will hopefully reduce the likelihood that the patient will degenerate in a lethal vfib.9–14
TWELVE-LEAD ELECTROCARDIOGRAPHY
The actual 12-lead ECG that we know today was developed by Emmanuel Goldberger in 1942 (refer to the history of the ECG in Table 11-1 to appreciate the efforts of many others)1–7 and allows for a more detailed and systematic examination of the ECG and specific disorders that may affect the ECG. As previously mentioned, each ECG electrode provides a view of the electrical activity of the heart under which the ECG electrode lies.
The ECG leads that produce the 12-lead format include the limb leads (leads I through III, aVR, aVL, aVF) and the precordial leads (V1 through V6), which are shown in an ECG from a normal heart in Fig. 11-26. Note that they are arranged upon the page in a systematic, standardized manner. The limb leads occupy the left half of the page, and the precordial leads occupy the right half of the page. Note also that three heat styluses are vertically arranged one on top of the other, which allows the simultaneous recording of three leads. Leads I, II, and III (reading from top to bottom) are recorded at the same time; then, aVR, aVL, and aVF (reading from top to bottom). V1, V2, and V3 and V4, V5, and V6 are clustered in the same manner. It is important to note that this simultaneous recording allows the three different views of the same electrical event. This allows the practitioner to make judgment calls and clinical decisions about a particular ECG complex based on information obtained from three sources, and not just one. A simple count of these leads reveals that 12 different views of the heart’s electrical activity are provided in a typical 12-lead ECG. An ECG profile of a normal heart without a cardiac rhythm disturbance or disease is shown in Fig. 11-26. Each of these views was obtained from an ECG–electrode interface (a lead) that picked up the electrical activity of the heart and transported it through a series of wires to a circuit box (the proverbial “black box”), which processed the electrical activity so that it could be graphically displayed.9–13
FIGURE 11-26 The ECG leads that produce the 12-lead ECG include the limb leads (leads I through III, aVR, aVL, aVF), and the precordial leads (V 1through V6). Note the presence of calibration marks (arrow) and the notation “25 mm/s” reflecting a machine that is set to standard calibration.
VIEWS OF THE HEART: EINTHOVEN’S TRIANGLE
In order to understand the area of the heart that each limb lead looks at, it is important to understand something about Einthoven’s triangle. Willem Einthoven placed electrodes on both arms and both legs and used leads to connect them to a simple ECG recorder. He manipulated the polarity of each lead relative to the other leads and developed a triangle of polarity as shown in Fig. 11-27A. Each face of the triangle was given a numeric lead assignment, either I, II, or III. If the leads are all collapsed around an imaginary center, one develops a different figure, as shown in Fig. 11-27B. Note that each of these leads has a positive pole and a negative pole. Each of these leads is configured to “look toward” the positive pole. Thus, lead I “looks toward” the patient’s left, lead II “looks toward” the patient’s left leg, and lead III “looks toward” the patient’s right leg.
FIGURE 11-27 (A) Einthoven’s triangle. (B) The three limb leads derived from this triangle. (C) The current 6-lead system consisting of Einthoven and augmented leads, providing a view of the heart’s electrical activity every 30 degrees. (Only A reproduced with permission from Barrett KE, Barman SM, Boltano S, et al. Ganong’s Review of Medical Physiology. 23rd ed. New York: McGraw-Hill; 2010, Fig. 30-8.)
Now conceptualize a 360-degree circle that is superimposed on your own chest. Let us arbitrarily designate 0 degrees as looking toward the left arm, +90 degrees as looking straight down toward the floor, and +/− 180 degrees as looking toward the right arm. Similarly, − 90 degrees looks straight up toward your head, and 0 degrees looks once again toward your left arm and completes the circle.
The previous exercise allows the practitioner to assign a value in degrees to each of Einthoven’s three leads. Lead I looks toward 0 degrees, lead II looks toward 60 degrees, and lead III looks toward 120 degrees. This system allows the practitioner a view of the heart every 60 degrees.
The problem with Einthoven’s original scheme was that it was not specific enough to accurately pinpoint cardiac pathology. The development of the augmented lead system in 1942 changed that. The augmented lead system uses more than one lead as the negative pole and thus splits the difference between leads I, II, and III. This allows a view of the heart every 30 degrees.
As can be appreciated from Fig. 11-27C, lead aVR looks over the right shoulder, lead aVL looks over the left shoulder, and lead aVF looks straight down. An augmented lead thus alternates with an Einthoven lead.
In order to identify the location of cardiac pathology, it is important that the clinician learn where each of the six limb leads “looks.” This can be accomplished by recalling the 360-degree circle that was constructed over the anterior chest and the assignment of degrees beginning at 0 degrees on the left and moving to +/−180 degrees on the right. By recalling that an Einthoven lead alternates with a limb lead, it should be easy to divide the circle into 30-degree units and rotate around the lower hemisphere of the 360-degree circle, reciting “I-aVR-II-aVF-III-aVL” (see Fig. 11-27C).
Knowledge of the position of the heart within the chest is essential in understanding the area of the heart that each ECG lead records. Recall the position of the heart within the thorax. If the long axis of the heart is conceptualized as an arrow, then the shaft is a line formed by the interventricular septum, the point is the apex, and the atria are the feathers. This arrow is positioned such that the point is directed inferior, to the left, and anterior, while the feathers are directed superior, to the right, and posterior, toward the back. The heart is rotated on its long axis such that the left ventricle is to the left and the right ventricle is an anterior structure. The position of the heart is such that a large portion of the left ventricle is in direct contact with the diaphragm (called the inferior, or diaphragmatic, portion of the left ventricle).
Recall that the limb leads look at the heart’s electrical activity in the frontal plane and reflect cardiac electrical activity that lies beneath these leads. Thus, leads I and aVL look at the high lateral wall of the left ventricle; leads II, III, and aVF look at the inferior wall of the left ventricle; and lead aVR looks toward the right atrium. The previous information is vital in appreciating pattern recognition in patients with myocardial ischemia or infarct.
Data Acquisition from the 12-Lead ECG
The student should have some understanding of the manner in which a 12-lead ECG is obtained. This is best accomplished by reviewing the operation of a typical ECG recorder. Two such recorders are shown in Fig. 11-28.
FIGURE 11-28 Left, a modern 12-lead ECG machine. Right, the Hewlett-Packard 1500B 12-lead ECG system.
Limb Leads
The limb leads consist of leads I, II, III, aVR, aVL, and aVF and are obtained from the electrode–wire interfaces shown in Fig. 11-29A. The limb leads look at the heart’s electrical activity in the frontal plane. The electrodes of the ECG recorder are actually spring-loaded plastic grips, which have a small metal piece inside the plastic grip. Placing conductive gel on these metal pieces and then placing the grips on the limbs allow the electrical activity of the heart to be acquired. If the dial of the ECG recorder is set on limb lead I (Fig. 11-29B), it will acquire the electrical activity of the heart as it travels from the right arm to the left arm and will produce the tracing shown in Fig. 11-29Cthat is characteristic of limb lead I. Lead I looks toward 0 degrees and looks at the high lateral wall of the left ventricle. Similarly, if the dial of the ECG recorder is set on limb lead II, it will acquire the electrical activity of the heart as it travels from the right arm to the left leg and will produce a different tracing characteristic of limb lead II. Lead II looks toward 60 degrees and looks at the inferior wall of the left ventricle. Finally, if the dial of the ECG recorder is set on limb lead III, it will acquire the electrical activity of the heart as it travels from the left arm to the left leg and will produce the tracing that is characteristic of limb lead III. Lead III looks toward 120 degrees and also looks atthe inferior wall of the left ventricle.9–13
FIGURE 11-29 (A) Placement of the limb leads on a subject. (B) Setup of ECG acquisition in order to obtain lead I. (C) The resultant paper printout of lead I.
Leads aVR, aVL, and aVF form the augmented leads that subdivide Einthoven’s leads and provide a view of the heart’s electrical activity every 30 degrees. When the dial of the ECG recorder is set on aVR, it will acquire the electrical activity of the heart as it travels to the right arm and will produce a tracing that is characteristic of lead aVR. It should be noted that in a normal tracing (Fig. 11-26), all the ECG waveforms in aVR are inverted. This is because the positive electrode of aVR looks over the right shoulder; because the vector is moving down and to the left (ie, down the normal conduction pathway), the vector is moving away from a positive electrode and therefore inverts the P, QRS, and T waves. When the dial of the ECG recorder is set on aVL, it will acquire the electrical activity of the heart as it travels to the left arm and will produce a tracing that is characteristic of lead aVL. Finally, when the dial of the ECG recorder is set on aVF, it will acquire the electrical activity of the heart as it travels to the left foot and will produce a tracing that is characteristic of lead aVF. It should be noted that normally the waveforms in aVF are strongly positive; this is because the positive electrode of aVF looks straight down; because the vector is moving down and to the left (ie, down the normal conduction pathway), the vector is moving toward a positive electrode and therefore produces upright P, QRS, and T waves.11
Precordial Leads
The precordial leads are unipolar leads like the augmented voltage leads and consist of V1, V2, V3, V4, V5, and V6. The precordial leads look at the heart’s electrical activity in the horizontal (transverse) plane. The value of the precordial leads is the proximity each has to the heart (rather than the large distance in the augmented voltage leads presented immediately above) as well as the different views of the heart’s electrical activity that can be acquired as each lead traverses the left upper quadrant of the thorax. The position of each of the precordial leads is presented in Table 11-2 as well as Fig. 11-30.
TABLE 11-2 Location of the Precordial Electrodes on the Chest Wall
FIGURE 11-30 Standardized placement of the precordial leads across the chest in order to obtain V1 through V6.
Acquisition of V1 is accomplished by setting the dial of the ECG recorder on “V” and placing the suction cup in the fourth intercostal space, right parasternal border, as shown in Table 11-2. The ECG machine will acquire the electrical activity of the heart from the location of the suction cup. The suction cup is placed at each of the six standard precordial placement sites provided in Table 11-2 and will acquire the electrical activity from each of these sites. The acquired electrical activity of the heart from these six sites will produce the characteristic ECG complexes shown in Fig. 11-26, right side of the panel.
For the interpretation of the 12-lead ECG, it may be best to group the six precordial leads by their anatomical location (eg, the part of the heart that they overlie and from which the heart’s electrical activity is acquired).9–13Precordial leads V1 through V2 are typically considered to represent the electrical activity of the heart from an anterior perspective (or view) of the left ventricle, leads V3 through V4 are considered to provide an anteroseptal view of the electrical activity from the left ventricle, and leads V4 through V6 are considered to provide lateral views of the electrical activity from the left ventricle. A posterior view of the heart’s electrical activity is acquired from leads V1through V2 by examining these leads for inverse or reciprocal changes (often referred to as a mirror image) associated with the posterior wall of the left ventricle.9–13 The inferior wall of the left ventricle is the only area of the left ventricle not represented by the precordial leads. The inferior wall of the left ventricle can be examined in leads II, III, and aVF.9–13 The right ventricle can be appreciated by viewing right (rather than left) precordial leads.15,16Several right precordial leads that have been used in the past include precordial leads V3 through V6, but on the right of the sternum, as well as a right precordial lead, CR4R. The standard left precordial leads V1 and V2 as well as lead aVF have also been used to examine the right ventricle via electrocardiography. The ability to examine different aspects of the heart and different diseases by viewing specific ECG leads and characteristics will be further discussed in the following section.
The 12-Lead Electrocardiogram
The 12-lead ECG shown in Fig. 11-26 and in Figs. 11-31 through 11-34 is performed for many reasons. These include assessing the (1) likelihood of cardiovascular, pulmonary, or other diseases; (2) presence of cardiac rhythm disturbances; (3) likelihood of an acute or old myocardial infarction; (4) likelihood of atrial or ventricular hypertrophy; and (5) possibility of ECG changes over a certain period of time due to one or more of the aforementioned or other conditions (see Table 11-3). The methods to examine and interpret these particular findings are presented in the following section.
TABLE 11-3 Reasons to Perform a 12-Lead Electrocardiogram
FIGURE 11-31 Twelve-lead ECG representing an acute anteroseptal and lateral wall MI. Note the ST-segment elevation and the loss of R waves in V2 through V6 coupled with deep T wave inversions. Note also the loss of R waves in leads II, III, and aVF (a probable old inferior wall MI) with the resultant left axis deviation (LAD) of –60 degrees.
Use of the 12-Lead Electrocardiogram in Physical Examination
The preceding section highlights the important role the 12-lead ECG can play in the physical examination of patients seen by a physical therapist. Although these skills have been considered to be advanced,17 they are easily acquired and can aid in the examination and management of all types of patients seen in physical therapy. These clinical skills are particularly important for the Doctor of Physical Therapy (DPT) student and practitioner. The areas worthy of further attention include methods to (1) calculate the axis of the heart, (2) evaluate the likelihood of atrial and ventricular hypertrophy, and (3) identify signs of myocardial injury or infarction. These areas will be presented in the following sections.
Axis of the heart—The axis represents the sum total of all the electrical forces during any given cardiac cycle and the direction that the positive wave of depolarization takes as it travels from the SA node to the terminal fibers of the Purkinje system. The reader will recall the 360-degree circle superimposed on the patient’s chest that forms the landmarks against which the limb leads are derived. The positive electrode of lead I “looks at” the patient’s left, representing 0 degrees; aVF “looks” straight down at 90 degrees. These two landmarks will provide the basis for determination of axis. The procedure for this determination is represented in Box 11-2.
BOX 11-2
Estimation of Axis
1.Examine lead I (0 degrees). If the R wave is mostly positive, then it means that the positive wave of depolarization is heading toward lead I and that the axis must lie in the hemisphere whose center is 0 degrees.
2.Examine lead aVF (90 degrees). If the R wave is mostly positive, then it means that the positive wave of depolarization is heading toward lead aVF, and that the axis must lie in the hemisphere whose center is 90 degrees.
3.The area that both hemispheres have in common is a half-hemisphere wedge between 0 and 90 degrees. Therefore, the axis must lie somewhere between 0 and 90 degrees.
4.Examine all six limb leads. Find the lead that is the most isoelectric (ie, that demonstrates a balance between upward and downward deflection of the QRS complex.)
5.Recall that if the positive wave of depolarization travels perpendicular to a positive electrode, an isoelectric waveform is the result.
6.Construct the perpendicular to this lead. Use only that portion of the construct that falls between 0 and 90 degrees. The position toward which this new constructed lead points is an approximation of the true axis. See Fig. 11-31 for an example of an axis shift.
The mechanisms responsible for the axis of the heart include the position of the heart in the chest, the size of the heart, and the viability of the myocardium. As mentioned previously, the vector, or sum total of all the electrical forces developed during depolarization, travels through the normal conduction pathway in a downward and leftward direction. If a 360-degree circle is superimposed over the anterior chest, the normal axis of the heart is approximately 60 degrees or anywhere between 0 degrees and 90 degrees. The direction of the heart’s electrical axis can deviate from the normal value. Individuals who are unusually tall can have a “vertical heart” that places their axis at 90 degrees or more; obese individuals may have a “horizontal heart” that places their axis at 0 degrees or less because of the upward displacement of the heart and diaphragm brought about by expansion of the abdomen. Ventricular hypertrophy due to hypertension can increase left ventricular muscle mass and its electrical activity and can cause an axis deviation to the left, toward the hypertrophy. Finally, myocardial infarction can cause significant myocardial cell muscle death, which is replaced by nonconducting scar tissue. This causes an axis shift away from the lesion. Each of these mechanisms has a major influence of the determination of axis, but the position of the heart in the chest and the size of the heart and its respective chambers will have the greatest influence on the development and direction of the heart’s electrical activity. See Fig. 11-31 for an example of an axis shift away from an old inferior wall MI.
Atrial and ventricular hypertrophy—The likelihood of atrial and ventricular hypertrophy can be evaluated using a variety of methods that were presented in Chapter 10. Table 11-4 provides an overview of the different methods to evaluate atrial and ventricular hypertrophy using the ECG. Close examination of this table reveals that the key methods to evaluate the likelihood of atrial or ventricular hypertrophy are to measure the (1) duration of particular ECG intervals or segments and (2) magnitude of voltage in the R and S waves. The greater the hypertrophy, the greater the amount of time required for electrical activity to traverse hypertrophied myocardium, thus producing a prolonged or abnormal ECG interval or segment. Similarly, a greater amount of myocardial muscle mass will generate a greater amount of voltage and produce taller R waves or deeper S waves in particular ECG leads. It is also apparent from Table 11-4 that specific methods to differentiate left from right ventricular hypertrophy exist, but no such specific method exists to differentiate left from right atrial hypertrophy. However, it has been suggested that it may be possible to identify left atrial hypertrophy by the observation of a biphasic P wave in V1 that is characterized by the terminal portion of the P wave being 1.0 mm or more in depth and 0.04 seconds in duration.11
TABLE 11-4 Methods to Evaluate Atrial and Ventricular Hypertrophy via Electrocardiography
Table 11-5 provides two methods to quantify these measurements using the criteria established by Estes and Scott.17,18 Estes’s method assigns a certain number of points based on particular ECG findings, whereas Scott’s criteria simply use the voltage measurements of the R and S waves in the limb leads and several of the precordial leads.17,18 The practicing physical therapist may find that Scott’s precordial lead criteria offer the easiest way to assess for the presence of left ventricular hypertrophy.
TABLE 11-5 Scoring Methods to Predict Left Ventricular Hypertrophy
Myocardial injury or infarction—Identification of myocardial injury or infarction is also an ECG skill considered to be advanced, but simple observation of the ST segment and a few other ECG abnormalities can provide a wealth of information about injury or infarction to the myocardium.
CLINICAL CORRELATE
Physical therapists working with patients who have suffered a recent acute MI should follow the evolution or resolution of this event using serial ECG reports, which can provide valuable information that can be used to direct subsequent exercise strategies.
Table 11-6 provides an overview of the process used to examine the ECG for signs of myocardial injury or infarction. Identification of ST-segment depression and elevation as well as the significance and implications of both have been presented in the earlier portion of this chapter. Table 11-6 expands the role of measuring ST-segment depression or elevation in one single ECG lead presented earlier and presents the methods to characterize and group these and other measurements to localize specific areas of the heart that have been damaged, both acutely and long ago.
TABLE 11-6 Patterns of Recognition of Myocardial
It should be clear from Table 11-6 that particular patterns of injury or infarction can be observed with a 12-lead ECG. These patterns are dependent on the anatomy of the coronary arteries and the location of the ECG electrodes. In brief, these patterns of injury or MI include locations in the anterior, posterior, anteroseptal, lateral, and inferior areas of the heart. Some evidence exists that a superior pattern can also be identified, but this pattern is not universally accepted. These patterns of recognition, the ECG leads, and the underlying coronary anatomy that appear to be responsible for the aforementioned patterns are provided in Table 11-6.
The aforementioned process of pattern recognition can be appreciated in Fig. 11-31 in which the 12-lead ECG displays an acute MI and the evolutionary changes after several days of recovery. The acute MI is apparent in the anteroseptal precordial leads (V2, V3) and lateral precordial leads (V4, V5, V6) of Fig. 11-31 by the ST-segment elevation, representing a zone of injury. Also of note is the presence of T-wave inversions in I, II, and aVL, representing a zone of ischemia. This zone of ischemia represents jeopardized myocardium that could become necrotic over the next few days as the MI continues to evolve. Fortunately, the ischemic changes in this example normalized approximately 4 days later. Figure 11-32 demonstrates the presence of an older inferior wall MI, with characteristic changes in leads II, III, and aVF. Note the presence of deep Q waves in these leads, coupled with loss of the R waves. The Q waves represent areas of full-thickness myocardial necrosis, a change that usually evolves subsequent to the earlier ST-segment displacements seen in Fig. 11-31. In Fig. 11-32, note also the newly evolving MI in the anteroseptal area, as evidenced by the dramatic ST-segment elevations in the early and midprecordial leads, and the poor R-wave progression as one moves from V1 to V6.
FIGURE 11-32 Inferior wall MI, age indeterminate. Note the loss of R waves in II, III, and aVF. Note also the new anteroseptal wall MI, as evidenced by the deep Q waves in leads V1 through V3. This individual clearly has multivessel disease of both the right and the left coronary arteries.
CARDIAC PACEMAKERS
Cardiac pacemakers play an important role in the treatment of heart disease due to cardiac rhythm disturbances. They have the ability to pace the heart (ie, discharge an electrical stimulus to initiate a wave of depolarization throughout the heart). Pacemakers have a characteristic pattern that is easy to recognize on an ECG. The pacemaker produces its own wave of depolarization that marks the ECG with a pacer spike as shown in Fig. 11-33. Improved technologies have increased the application of pacemakers and pacemaker principles to the treatment of other types of heart disease including coronary artery disease and heart failure. Because the use of pacemakers has increased (and will likely further increase as technological advancements continue), as well as the potential role of physical therapy for persons with cardiac pacemakers, this section will be devoted to the cardiac pacemaker. This potential role includes assisting with the (1) establishment of pacing parameters (with electrophysiologic physicians) to obtain optimal functional and exercise outcomes and (2) establishment of safe functional and exercise activities for patients with pacemakers and automatic implanted cardioverter-defibrillators (AICDs). The indications for a pacemaker, types of pacemakers, as well as pacemaker codes and pacing modes will be presented so that the physical therapist can provide optimal physical therapy to patients with cardiac pacemakers.
FIGURE 11-33 ECG rhythm strip showing a pacemaker spike initiating a ventricular response. Note the failure to capture the ventricle (arrow) and the native rhythm that follows.
Indications for a Cardiac Pacemaker
The indications for a cardiac pacemaker are listed in Box 11-3 and include a sick sinus syndrome, complete heart block, or cardiac denervation as in cardiac transplantation. Several other indications exist and for each of these reasons the primary goal is to improve the synchrony of myocardial mechanics (chamber filling and emptying) to enhance cardiac function such as the stroke volume, cardiac output, and ejection fraction.
BOX 11-3
Indications for a Cardiac Pacemaker
1.Sick sinus syndrome
2.Complete heart block
3.Cardiac denervation as in cardiac transplantation
4.Severe cardiac rhythm disturbances
5.Easily provoked angina
6.Congestive heart failure
Types of Pacemakers
The types of pacemakers that are currently available are listed in Table 11-7. Four basic types of pacemakers exist and include fixed-rate pacemakers, demand pacemakers, atrial-triggered pacemakers, and ventricular-triggered pacemakers. The most common pacemakers are demand pacemakers, which pace the heart on demand and most frequently will pace the ventricle. To fully understand the pacemakers listed in Table 11-7, it is necessary to review the three-letter pacemaker codes, which have been expanded over the years to five-letter codes.
TABLE 11-7 Different Types of Pacemakers
Pacemaker Codes
The coding of pacemakers began in 1974 and outlined a three-letter coding sequence, which made it easy for one to understand the cardiac chamber being paced (the first letter of the code and can be an A for atrium, V for ventricle, or D for dual atrium and ventricle), the cardiac chamber being sensed (the second letter of the code and can be an A for atrium, V for ventricle, D for dual atrium and ventricle, or O for none), and the mode of response (the third letter of the code and can be I for inhibited, T for triggered, D for atrial triggered and ventricular inhibited, R for reverse, or O for none). Because the initial 3-letter code was introduced, two additional codes have been added to keep pace with the technological advancements applied to pacemakers. The two additional codes represent programmability (the fourth letter of the code and can be a P for programmable rate and/or output, M for multiprogrammable, or O for none) and tachyarrhythmia functions (the fifth letter of the code and can be a B for burst, N for normal rate competition, S for scanning, E for externally activated, or O for none). It is now apparent that adding these two additional codes to the original 3-letter code system produces a 5-position pacemaker code.
Each of the specific letters within each of the code positions after the second letter is related to specific actions of the pacemaker, which gives it greater or lesser clinical utility. Table 11-7 alludes to this, but further discussion of the actual pacing modes is needed to fully appreciate pacemaker capabilities and the role of the physical therapist when working with patients who have received a permanent pacemaker.
Pacing Modes
The available pacing modes can be interpreted from Table 11-7. A quick review of the actual available modes of pacing should facilitate a better appreciation for the pacemaker. Table 11-7 identifies three of the listed pacemakers as obsolete. The reason for this is due to the rather primitive mode of pacing, a fixed rate of pacing of either the atria or the ventricle.
The second type of pacemaker listed in Table 11-7 is the P-triggered ventricular pacemaker that has a VAT coding. The V indicates that the cardiac chamber being paced is the ventricle, A indicates that the cardiac chamber sensing the electrical activity in the heart is the atria, and T indicates that the mode of response is to trigger a paced beat in the ventricle when the atrium senses the SA node’s wave of depolarization that cannot proceed past the AV node. This type of pacemaker is used in patients with normal SA node function and without bradycardia or atrial tachyarrhythmias (because with this type of pacemaker it is the role of the atria to signal the pacemaker to discharge an action potential to the ventricle). When the pacemaker sensor in the atria senses electrical activity, it triggers the pacemaker to pace the ventricle at a rate commensurate with the normal and needed atrial rate of discharge from the SA node. This is truly a physiologically favorable pacing mode. It is also easy to understand why a patient with bradycardia or atrial tachyarrhythmias would not be a good candidate for such a pacemaker, because the pacemaker would be pacing the ventricle either too slow or too fast. The atrial-synchronized, ventricular-inhibited pacemaker (with an ICHD code of VDD) and the QRS-triggered and -inhibited ventricular pacemakers (with ICHD codes of VVT and VVI, respectively) function in much the same way as the P-triggered ventricular pacemaker (with VAT code), only they sense from the atrium and ventricle (for the VDD pacemaker) or the QRS wave from the ventricle (for the VVT and VVI pacemakers), but all similarly pace the ventricle.
The demand AV sequential pacemaker with an ICHD coding of DVI is another type of pacemaker that attempts to provide more physiologically sound pacing (like the P-triggered ventricular pacemaker). It attempts to synchronize the atrial and ventricular electrical activity of the heart, which may result in better mechanical activity of these cardiac chambers and improved cardiac function. This pacemaker is used in patients with atrial bradyarrhythmias with or without impaired AV node function. It is not used in patients with prolonged bouts of atrial fibrillation or flutter. When a patient with this DVI coded pacemaker experiences sinus bradycardia, the ventricle senses a need to pace the atrium and ventricle (the “D” code) and inhibits pacing when the ventricle no longer senses sinus bradycardia. Despite the fact that this pacemaker attempts to pace the heart in a truly physiologic manner, it is unable to (1) alter the paced rate (the heart rate) to increased physiologic demands and (2) maintain AV synchronous pacing during periods of normal sinus rhythm and AV block.
The last pacemaker listed in Table 11-7 is the universal, fully automatic pacemaker with DDD coding. The DDD pacemaker is used in patients with (1) atrial bradyarrhythmias with or without impaired AV node conduction and (2) normal sinus node function, but with impaired AV node conduction. When a patient with this DDD-coded pacemaker experiences sinus bradycardia or impaired AV node conduction, either the atrium or ventricle senses (the second “D” code) the abnormality and inhibits pacing where pacing was sensed and then triggers either the atria or ventricle to pace in the chamber where no electrical activity was sensed (the first “D” code). Although there are really no significant disadvantages to the universal, fully automatic pacemaker, the other pacemakers presented previously have several important advantages and disadvantages that are worthy of further discussion. This discussion will hopefully further clarify the modes and mechanism of action of pacemakers.
Advantages and Disadvantages of Available Pacing Modes
The advantages and disadvantages of the currently available pacing modes are listed in Table 11-8. It is apparent from this table that the patient with a pacemaker other than the universal, fully automatic pacemaker will likely have limited cardiac function due to suboptimal AV contraction (and other characteristics inherent in the different types of pacemakers), which is likely to affect functional activities. Because of this and other pacemaker issues, the next section will present a more complete listing of pacemaker modes and functions (rate modulation, cardiac resynchronization therapy [CRT], and implantable cardioverter defibrillator [ICD] therapy).
TABLE 11-8 Advantages and Disadvantages of Different Pacemakers
Additional Pacemaker Modes and Functions
Table 11-9 provides an overview of the pacemaker codes previously reviewed as well as two additional symbols that have become increasingly important in the management of patients requiring a pacemaker. The two additional symbols sit in the fourth and fifth positions of the pacemaker code. The fourth symbol identifies the programmable rate modulation function of the pacemaker while the fifth symbol identifies the anti-tachyarrhythmia function of the pacemaker. Pacemakers with letters in these positions have one of more of the functions listed in Table 11-9.
TABLE 11-9 Pacemaker Code Classificationa
Rate modulation—Rate modulation refers to the pacemaker’s ability to modulate heart rate based on activity or physiologic demands.19–23 Pacemakers usually are fit with one or two (dual) sensors including various derivatives of two methods consisting of (1) activity or motion based and (2) physiological based with the most common sensor being one that measures minute ventilation. The sensors and pacemaker attempt to promote a normal sinus node response to increasing HR with exertional demands.24
The type of sensor(s) utilized may impact the ability of the pacer to respond to various exercise modalities.25 Motion/activity sensors result in sluggish HR response to activities that are smooth such as on the bicycle ergometer or with supine, seated, or standing exercise, and rapid response to ambulation. However, these pacers have poor proportionality (ie, faster rates when descending stairs than when ascending) and poor specificity (ie, inappropriate high rates when riding over a bumpy road).26 In patients with motion sensors, activities that promote movement of the thorax (hallway ambulation) or treadmill protocols that include increases in both speed and grade, should be utilized to trigger an increase in HR. QT sensors and ventilatory driven sensors may require longer warm-up periods because of delayed responses to activity; however, these sensors have good proportionality and specificity. QT sensors are the only sensors that respond to emotional stress; however, medication and electrolyte level changes may impact responsiveness of HR with QT interval sensors.26
Combinations of sensors, or dual sensor rate modulation pacers, seem to offer the best HR response to immediate activity demands by exploiting strengths and counteracting weaknesses of individual sensors. Ventilation sensors provide the predominant contribution during intense effort with activity sensors failing to reach required HRs for optimal hemodynamic response.27–30
The upper limit of the pacemaker rate modulation should be known since blood pressure may not be adequately maintained if the upper limit is exceeded. Thus, blood pressure should be properly monitored in patients with pacemakers that have been programmed to provide rate modulation. Increases in heart rate above the upper limit of the pacemaker modulation rate will stimulate the pacemaker to introduce a Wenckebach (Mobitz I) atrioventricular heart block rhythm that can result in reductions in blood pressure and shortness of breath. The best mechanism to identify such a phenomenon may be to simply monitor the ECG during exercise.31
While the majority of pacemakers implanted in the United States generate a rate response, not all pacers are equipped with rate modulation, and therefore some patients have heart rates that may not change with activity. In patients with pacemakers not equipped with rate modulation, low-level activity with small incremental increases in metabolic demand are preferred. Assessment of RPE, blood pressure, and symptoms should be utilized to monitor tolerance to exercise.
Implantable cardioverter-defibrillators—The use of pacemakers and implantable cardioverter defibrillator (ICD) therapy has increased considerably over the past decade because of the lifesaving defibrillation provided to patients with fatal arrhythmias as well as one or more of the indications listed in Table 11-10.19,32–44 Despite the mostly favorable effects of ICD therapy (defibrillating a patient who experiences a life-threatening cardiac arrhythmia), patients with ICD have significant psychological ramifications from the possibility of sudden defibrillation and frequently limit their functional and exercise activities in fear of defibrillation.32–34 Support groups for patients with ICD appear to help decrease the anxiety and fear associated with ICD therapy.
TABLE 11-10 Indications for an Implantable Cardioverter-Defibrillator
Only through the actual performance of functional and exercise tasks can a patient realize their functional and exercise abilities, which highlights the important role for physical therapists in the care of persons receiving ICD therapy.24–34,45–47 The physical therapist’s role in the examination and management of patients with ICD can be substantial and could include one or more of the tasks outlined in Table 11-11. Of these tasks the most important are likely to understand the reasons for ICD implantation and each patient’s ICD discharge heart rate for defibrillation. Maintaining the patient’s heart rate below the ICD discharge heart rate will prevent defibrillation that may occur accidentally due to the increase in heart rate from exercise. However, newer and more sophisticated pacemakers with ICD capacity are able to interrogate the morphology of the heart rhythm and differentiate an expected sinus tachycardia during exercise from a fatal ventricular tachycardia.
TABLE 11-11 Potential Role of Physical Therapists for Patients with Implantable Cardioverter-Defibrillators
Finally, it has been reported that inappropriate discharge of an ICD may occur from transcutaneous electrical nerve stimulation (TENS) and other electromagnetic therapy that may be provided by a physical therapist.36–39 Thus, it is important to obtain a comprehensive history of a patient known to have a pacemaker to determine if it has ICD capacity. Physical therapists should consult with referring physicians before providing patients with an ICD pacemaker with any form of electromagnetic therapy.
For example, several case reports exist whereby neuromuscular electrical stimulation (NMES) has resulted in electromagnetic interference causing false sensing and leading to inappropriate defibrillation in patients with AICDs, which results in cardiac arrhythmias or painful shocks.36–39 Interference has been observed during both NMES of the trapezius and the quadriceps of patients, indicating that individual testing for interference is warranted before NMES should be utilized in patients with ICDs. Electromagnetic energy (EME) from household devices, airport security, and cell phones can also cause inappropriate shocks and interfere with pacemaker function by either creating a sensed beat or delaying the sequence of a paced beat. Patients should be advised to discuss the possibility of EME with their cardiologist since the major determinant of response is based on the manufacturer of their device. Some general guidelines include the following: the potential for EME is proportional to the strength of the environmental source; the closer the source to the implantable device, the greater the risk (with <10 cm distance even cell phones can create EME—therefore, patients are advised to use cell phones on the side opposite of the implantable device); security systems are usually safe as long as the patient does not linger at the source; and security staff should be advised of the location of an implantable device to avoid bringing a electromagnetic wand within close proximity.36–39
Cardiac resynchronization therapy—Cardiac resynchronization therapy (CRT) is a medical treatment that is used to synchronize the electrical, physiologic, and mechanical events of the heart via a pacemaker.48–52 It has become useful in the management of patients with heart failure.
A simplified explanation of CRT is the process that is used to synchronize AV as well as right and left ventricular depolarization and contraction in hopes of eliciting a more efficient and effective cardiac contraction. Although CRT has been a potential therapeutic modality for the past 6 to 8 years, it is only now receiving greater clinical use. This is surprising in view of the benefits that have been observed in much of the CRT literature, which has been summarized in Table 11-12.48–52 Furthermore, several important predictors of mortality have also been improved with CRT including left ventricular size, norepinephrine levels, heart rate and heart rate variability, peak oxygen consumption, New York Heart Association classification, and 6-minute walk test distance ambulated.48–52 Although the improvements in these important indices of survival in CHF are noteworthy, investigation of the specific effects of CRT on mortality are needed. Nonetheless, the improvements in many of the manifestations of CHF shown in Table 11-12 are likely to improve the functional abilities and quality of life of individuals with CHF.48–52
TABLE 11-12 Potential Beneficial Effects of Cardiac Resynchronization Therapy on the Manifestations of Chronic Heart Failure
The beneficial effects of CRT in persons with CHF are likely due to the combined effects of numbers 1 to 5 in Table 11-12. The improvements in atrioventricular conduction; ventricular filling, activation and contraction; and improved ventricular wall motion likely produce the remaining beneficial effects (numbers 6–12) in Table 11-12.17–22 Despite the potential beneficial effects of CRT on the manifestations of CHF, there are several potential adverse effects of CRT in persons with CHF including infection, bleeding disorders, pacemaker dysfunction, and possibly increased arrhythmias.
Pacemakers and Physical Therapy
As mentioned previously, the potential role of physical therapy in the care of persons with pacemakers includes assisting with the (1) establishment of pacing parameters (with electrophysiological physicians [EP]) to obtain the best functional and exercise outcomes and (2) establishment of safe functional and exercise activities for patients with pacemakers and AICDs. An additional role for the physical therapist may be consultation with an EP to determine the type of pacemaker to be implanted in a patient based on functional and exercise tasks examined by the physical therapist. The methods by which a physical therapist may provide optimal physical therapy to patients with cardiac pacemakers and AICDs are presented in Table 11-13. The typical pacemaker ECG tracing is shown in Fig. 11-33. It is important to note that the pacemaker is easy to identify by the presence of one or more pacer spikes such as those shown in Fig. 11-33. The absence of a pacer spike in a patient who previously demonstrated such a spike may indicate pacemaker malfunctioning or pacing alterations. Likewise, pacer spikes in locations of the cardiac cycle where they should not be may be suggestive of pacemaker malfunctioning. If such ECG findings are observed and are accompanied by increased symptoms and decreased functional abilities, pacemaker malfunctioning is highly likely. In either case, consultation with EP physicians may be needed to better understand the goals of the EP physicians and to contribute to a patient’s overall care.
TABLE 11-13 Methods to Provide Optimal Physical Therapy to Patients with Pacemakers
CLINICAL CORRELATE
Perhaps the best methods of contributing to the care of patients with pacemakers are to monitor (1) the ECG for signs of pacemaker failure, (2) the ECG at rest and during exercise or functional tasks, (3) symptoms (eg, shortness of breath, Borg rating of perceived exertion) at rest and during exercise or functional tasks, and (4) the systolic and diastolic blood pressure at rest and during exercise or functional tasks.
Much of the methodology presented in the cardiac examination chapter (Chapter 10) applies to the patient with a cardiac pacemaker, but evaluation of symptoms and the cardiovascular response to exercise or functional tasks is critically important in the pacemaker patient. In fact, examination of symptoms and the cardiovascular response of a patient with a pacemaker can provide important information to EP to help to establish optimal pacemaker-sensing and pacing modes. Observing a patient’s symptoms, cardiovascular response, and achieved workloads or duration of exercise, we can identify the best pacemaker settings for a particular patient. This type of direct physical therapist–physician consultation and teamwork are likely to maximize a patient’s full potential in the realms of cardiovascular and functional outcomes.
“OTHER” IMPORTANT APPLICATIONS OF THE ELECTROCARDIOGRAM
Segmental/Interval Analysis
Specific segments or intervals of the ECG complex have significant clinical utility that provides important diagnostic, prognostic, and possibly even therapeutic information (ie, identification of a particular ECG pattern within the interval may guide physical or medical therapies). Because of this, a cursory overview of several of these segments and intervals will be provided below.
PR Interval
As previously mentioned, the PR interval provides information about the wave of depolarization traveling from the SA node to the AV node. It can provide information about conduction that is too fast or too slow and is measured in the manner shown in Fig. 11-5. The PR interval is measured by simply placing a heart rate ruler with a special PR interval ruler section, using a calipers, or counting the number of boxes between the beginning of the P wave to the beginning of the QRS complex as shown in Fig. 11-5. The measured PR interval can then be compared to the normal range for a PR interval (0.12–0.20 seconds). Conduction that is too slow is represented by a prolonged PR interval and was discussed earlier. Conduction that is too fast is represented by a shortened PR interval (<0.12 seconds). This shortened PR interval may produce rapid rhythm disturbances that may be life-threatening. In fact, this characteristic ECG abnormality has been given the name Wolff–Parkinson–White syndrome (WPW).
Wolff–Parkinson–White syndrome—WPW is caused by the presence of fast conducting accessory tracks that bypass the AV node. It is a syndrome characterized by rapid depolarization and is evident by a shortened PR interval that may or may not have an upward slope (delta wave). The presence of WPW is associated with rapid atrial rhythm disturbances and the identification of the shortened PR interval and delta wave should alert the clinician that rapid atrial rhythm disturbances may occur during physical therapy examinations or treatments.
QRS Interval
The QRS interval provides information specific to the manner by which the wave of depolarization travels through the ventricles, culminating in ventricular depolarization and contraction. Several specific abnormalities of the QRS interval can be identified in the ECG and can help to provide important diagnostic and prognostic information. Some of this information was alluded to in the earlier discussion of hypertrophy and the axis of the heart. The QRS interval can provide information about interventricular conduction delays (IVCD) and bundle branch blocks (BBB).
Interventricular conduction delays—Interventricular conduction delays (IVCD) simply indicate that the wave of depolarization through the ventricles is slowed, which may be due to a number of factors but commonly is due to scarring and blocked electrical pathways or abnormal routing of the wave of depolarization via other pathways.
Bundle branch blocks—Bundle branch blocks (BBB) are an extension of an IVCD with a very characteristic pattern seen best on 12-lead ECG. The right BBB is best identified by examining leads V1 and V2 for a “rabbit-ear” appearance in the R wave. In fact, the “rabbit-ear” appearance is the result of two distinct R waves that are displayed on the ECG in leads V1 and V2 because the blocked right bundle branch causes the wave of depolarization to travel to only the left bundle, which causes the anterior precordial leads on the chest (V1 and V2) to receive two interrupted waves of depolarization (the first one from the left bundle branch and the second from the blocked right bundle branch), which is delayed and traverses the right bundle area through an alternate route and arrives after the initial wave of depolarization via the left bundle branch.
Figure 11-34 displays a left BBB. The left BBB is best identified by examining leads V5 and V6 for a wide, bizarre-looking QRS complex (resembling a PVC). When a wide, bizarre QRS complex is seen in leads V5 and V6 and is accompanied by an IVCD, the subject is diagnosed with a left bundle branch block (Fig. 11-34). The IVCD and a wide, bizarre QRS complex are the result of a blocked left bundle branch that requires the wave of depolarization to travel through the right bundle branch, which takes a longer period of time that is best seen in the lateral precordial ECG leads (V5 and V6).
FIGURE 11-34 Twelve-lead ECG showing left bundle branch block. Note the wide QRS complexes that look like PVCs. Note also that each QRS complex is preceded by a P wave, which rules this possibility out.
QT Interval
The QT interval is another parameter that provides important information about the effects of particular medications on the electrical activity of the heart as well as a patient’s prognosis. The QT interval is measured by placing a heart rate ruler with a special QT interval ruler section, using a calipers, or counting the number of boxes between the Q wave and the end of the T wave as shown in Fig. 11-4. The measured QT interval should then be compared to the estimated QT interval, which is closely related to the heart rate. The QT interval decreases as heart rate increases. Therefore, the measured QT interval should be compared to the estimated QT interval for a particular heart rate. Table 11-14 provides the estimated QT intervals for a given heart rate. The estimated QT interval for heart rates greater than 100 bpm should be less than 0.27 to 0.35 seconds.
TABLE 11-14 Estimated QT Intervals Based on a Given Heart Rate
R wave height—As previously mentioned in the myocardial injury and infarction section of this chapter, the height of the R wave can provide information about damaged myocardial tissue. The sudden disappearance of an R wave in an ECG lead that had consistently been observed to have an R wave is a sign suggestive of an MI. This sign is due to the inability of the area of the MI to generate and transmit a wave of depolarization.
In addition to this sign of MI, the actual height of the R wave has been suggested to yield important information regarding myocardial contractility and filling pressures of the chambers of the heart. It has been hypothesized that the R wave of a heart that is contracting poorly (and producing elevated filling pressures within the cardiac chambers) will increase, whereas the R wave of a heart that is contracting normally will not change appreciably or will decrease. It is quite easy to measure the height of the R wave before and after an exercise test, a bout of exercise, or a functional task. Simply measuring the height of the R wave from the isoelectric line to the top of the R wave will yield a measurement that can be recorded and compared before and after an exercise session. It is important to note that the R-wave measurements of one session should not be compared to those of another session during which the ECG electrodes have been replaced. Replacement of the ECG electrodes may be responsible for changes in the height of the R wave when comparing the results of one exercise session to another session. The clinical significance of the change in height of the R wave appears to have some clinical utility in the examination of patients with suspected heart disease. It is another ECG finding that may be helpful in evaluating the likelihood of heart disease in an exercising patient and should be examined with many of the other variables previously presented in this chapter and in Chapter 10 (such as ST-segment depression, heart rate, blood pressure, and symptoms).
Heart Rate Variability
Heart rate variability involves the examination of fluctuation between ECG complexes. The fluctuation between ECG complexes is the result of several interrelated dynamic processes including breathing, nervous system activation, and cardiovascular performance. Perhaps the most important finding from heart rate variability research is that a healthier heart has greater fluctuation between ECG complexes, whereas an unhealthier heart has less fluctuation between ECG complexes. The simplest and first method used to examine heart rate variability is obtained by measuring the regularity between the ECG complexes using the caliper method previously described and shown in Fig. 11-6. Today, many ECG devices such as Holter monitors, ECG acquisition systems, and even the Polar Heart Rate Monitor can examine the fluctuations between ECG complexes and provide useful output data to evaluate a patient’s cardiovascular risk. Examining heart rate variability via either the caliper method (previously described) or the Polar Heart Rate Monitor may be the most clinically efficacious methods for a physical therapist. The methods previously described and shown in Fig. 11-5 and the equipment shown in Fig. 11-35 (the Polar HR Monitor) should provide the physical therapist with the mechanisms needed to measure and assess a patient’s cardiovascular risk using heart rate variability.
FIGURE 11-35 The Polar Heart Rate Monitor can provide the physical therapist with the mechanisms needed to measure and assess a patient’s cardiovascular risk before, during, and after exercise as well as using the mode to measure heart rate variability. (Manufactured by Polar Electro, Inc., Woodbury, NY.)
SUMMARY
This chapter has provided an overview of electrocardiography. It has been presented from a clinical perspective with valuable techniques for acquiring the electrical activity of the heart. Newer methods of acquiring the electrical activity of the heart (via the Polar Heart Rate Monitor) have also been presented in hope that these techniques may be employed by physical therapists interested in better understanding patient prognosis and response to therapeutic interventions. The most important principles of ECG interpretation are likely the measurement of heart rate, rhythm, and axis as well as the evaluation of myocardial injury, infarction, and hypertrophy. The methods to perform these relatively easy and basic skills have been described in the text and outlined for clarity within the tables of this chapter. Numerous examples of single-lead and 12-lead ECGs and methods to interpret them have also been provided.
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