Part I: Basic Principles and Patterns

Chapter 1: Essential Concepts: What is an ECG?

Review
An electrocardiogram (ECG or EKG) is a graphical (voltage as a function of time) recording of some of the electrical activity generated by heart muscle cells. The electrical signals are detected by means of metal electrodes. For a standard 12-lead ECG the electrodes are placed on the patient’s chest wall and extremities. The electrodes function as sensors and are connected to an instrument termed the electrocardiograph. The heart’s low amplitude electrical signals, which are detected, amplified, and displayed the electrocardiograph (ECG machine), represent only those produced by the working (contracting) atrial and ventricular muscle fibers (myocytes). The analysis of these recordings, from basic science and applied clinical perspectives, defines the field of electrocardiography or electrocardiology. This major area of modern medicine, in turn, falls under the more general rubric of cardiac electrophysiology.
In highly simplified terms, the heart can be conceptualized as an electrically timed, biologic pump whose activity is modulated by the autonomic (parasympathetic and sympathetic divisions) nervous system and other regulatory control mechanisms. The initiation of cardiac contraction by electrical stimulation is a key event setting off the complex set of processes referred to as electromechanical coupling. A fundamental aspect of the contractile (pumping or squeezing) mechanism is the release (and then reuptake) of calcium ions inside the atrial and ventricular heart muscle cells (myocytes). This process is triggered by the spread of the electrical activation signal through the atria and then the ventricles.
Normally, the cardiac stimulus starts in pacemaker (automatically and repetitively firing) cells of the sinus node. This network of specialized pacemaker cells, also termed the sinoatrial (SA) node, located in the high right atrium near the opening of the superior vena cava. From the SA node, the electrical stimulus (signal) spreads downward and to the left, through the right and left atria, and reaches the atrioventricular (AV) node, located at the bottom of the interatrial septum and near the top of the interventricular septum. After a delay, the stimulus spreads through the AV junction (comprising the AV node and bundle of His).
The bundle of His then subdivides into right and left bundle branches. The right bundle branch extends down the interventricular septum and into the right ventricle. From there the small Purkinje fibers rapidly distribute the stimulus outward into the main muscle mass of the right ventricle. Simultaneously, the left main bundle branch conveys the stimulus down the interventricular septum to the muscle mass of the left ventricle, also by way of the Purkinje fibers.
This recurring sequence of stimulation and recovery of the heart defines the normal physiologic processes cardiac electrical signaling. Disturbances of intrinsic pacemaker function (automaticity) and impulse propagation/recovery may result in cardiac arrhythmias and conduction disturbances.

Chapter 1: Questions
1. What is the normal (intrinsic) pacemaker of the human heart?
2. Identify the major components of the cardiac electrical signaling system.

3. What is the difference between an electrocardiogram and an electrocardiograph?
4. True or false: The ECG may provide clues about certain life-threatening electrolyte abnormalities and drug toxicities.
5. True or false: The ECG directly records only the electrical activity of working heart muscle cells (myocytes), not that of the SA node pacemaker cells or of cells comprising the specialized conduction system (AV node and His–Purkinje system).

Chapter 1: Answers
1. The collection of cells composing the sinus or sinoatrial (SA) node, located in the high right atrium near the opening of the superior vena cava.
2. Click on accompanying figure for answers

Chapter 2: ECG Basics: Waves, Intervals, and Segments

Review
The electrocardiogram (ECG), whether normal or abnormal, records two basic physiologic processes: depolarization (activation) and repolarization (recovery).

1. Depolarization: spread of stimulus through the heart muscle. This process produces the P wave from the atria and the QRS complex from the ventricles.
2. Repolarization: return of stimulated muscle to the resting state. This process produces the atrial ST segment and T wave (which are normally not seen on the surface ECG) and the ventricular ST segment, T wave, and U wave. The latter is usually a very small (≤1 mm) deflection just after the T wave. In important pathologic states (e.g., hypokalemia and with certain drug toxicities) prominent U waves may occur. Very prominent U waves are noteworthy because they are associated with increased risk of cardiac arrest from torsades de pointes ventricular tachycardia (see Chapter 16).

The five alphabetically named ECG waveforms are the P wave, QRS complex, ST segment, T wave, and U wave, occurring sequentially. ECG interpretation requires careful assessment not only of these waveforms themselves but also of the times within and between them.
Intervals are the portions of the ECG that include at least one entire waveform.
Segments are the portions of the ECG bracketed by the end of one waveform and the beginning of another.
The ECG in sinus rhythm is divisible into four major sets of intervals, defined as follows:

1. PR interval: from the beginning of one P wave to the beginning of the next QRS complex.
2. QRS interval (duration): from the beginning of one QRS complex to the end of the same QRS.
3. QT and QTc intervals: from the beginning of one QRS to the end of the subsequent T wave. Note: the QT interval is routinely corrected (adjusted) for the heart rate, and the designation QTc is used.
4. RR and PP intervals: from one point (sometimes called the R-point) on a given QRS complex to the corresponding point on the next. The instantaneous heart rate (beats per min) = 60/RR interval (in sec). Note: in sinus rhythm with normal (1:1) AV conduction, the PP interval will be the same as the RR interval. However, as discussed in later sections, the PP interval may be different from the QRS interval in certain AV conduction disturbances and cardiac arrhythmias.

The ECG recording in sinus rhythm is also divisible into three major segments, defined as follows:

1. PR segment: from the end of one P wave to beginning of the subsequent QRS complex. Atrial repolarization, which begins in this segment, continues during the QRS and usually ends during the ST segment.
2. ST segment: from the end of one QRS to the beginning of the subsequent T wave. As noted previously, the ST-T complex (waveform) is often considered as the earliest component of ventricular repolarization.
3. TP segment: from the end of one T wave to the beginning of the next P wave. This interval, which represents electrical diastole (resting state), is important because it is used as the isoelectric baseline reference from which to assess PR and ST segment deviations.

These basic ECG events are recorded on special graph paper divided into grid-like boxes. Each small box is 1.0 mm2. At the conventional recording (“sweep”) speed of 25 mm/sec, each millimeter horizontally represents 40 msec (0.04 sec). Each 200-msec (0.2-sec) interval is denoted by a thicker vertical line.
ECG recordings are also standardized such that a 1-mV signal usually produces a 10-mm deflection. Therefore, each millimeter vertically represents 0.1 mV. Each 5-mm (0.5-mV) interval is denoted by a thicker horizontal line. (Different voltage or temporal calibrations may be employed in special circumstances: e.g., 5 or 20/mV, or 50 or even 100 mm/sec.)

Chapter 2: Questions
1. What key electrophysiologic event occurs just before the sinus P wave appears?
2. To what fraction of a second does the smallest time division on the conventional ECG (recorded at a “sweep speed” of 25 mm/sec) correspond?

Chapter 2: Answers
1. Sinoatrial (SA) node depolarization, which is not recorded by the surface ECG. The P wave is generated by depolarization of atrial muscle, which is normally initiated by SA node depolarization.
2. 40 msec (0.04 sec) = 1/25 of a second. This very short amount of time (“blink of an eye”) highlights the capability of the ECG to capture physiologically meaningful events and pathologic changes that occur within fractions of a second, contributing to the importance and uniqueness of this clinical test.

Chapter 3: How to Make Basic ECG Measurements

Review
Because the electrocardiogram (ECG) graph is calibrated (standardized), its components (features) can be quantified by their amplitude (magnitude) and sign (positive or negative voltage) and by their width (duration). For clinical purposes, with the standardization set at its usual value of 1 mV = 10 mm, the absolute amplitude of a given waveform is generally reported in millimeters, not millivolts.
As described in Chapter 3, clinicians assess four basic sets of intervals:

1. RR (and PP) intervals. The atrial and ventricular heart rates are inversely proportional to the PP and RR (QRS–QRS) intervals, respectively. The longer/shorter the interbeat interval, the slower/faster the rate.

Cardiac rates are usually reported in units of beats or cycles/min. The ventricular (and atrial) rates are normally identical and can be quickly calculated in two ways:
Method 1 (box counting): Count the number of large (200 msec) time boxes between two successive R waves, and divide the constant 300 by this number. If you want a more accurate measurement of the instantaneous rate, divide the constant 1,500 by the number of small (40 msec) time boxes between two successive R waves.
Method 2 (beat counting): Count the number of QRS complexes that occur every 10 sec (the amount of data recorded on each page of most contemporary 12-lead devices) and multiply this number by 6. This method provides a useful measure of the short-term average heart rate over a given period. (You can do the same calculation for the atrial rate when this is different from the ventricular rate, as in second- or third-degree AV blocks, or in atrial tachycardias with block.)

2. The PR interval, which normally ranges from 120 to 200 msec (0.12-0.2 sec).
3. The QRS interval (or QRS duration), which is normally 100 msec (0.10 sec) or less, when measured in any given lead by eye. By electronic (computer) measurement, the upper limit of QRS duration is slightly longer at about 110 msec (0.11 sec).
4. The QT interval, which normally varies inversely with heart rate, becoming shorter as the heart rate increases, and vice versa. A variety of formulas, some given in the text, have been proposed for computing a rate-corrected QT, or QTc, interval; none is ideal.

Chapter 3: Questions
1. Abnormally slow conduction in the atrioventricular (AV) node is most likely to cause which of the following?
a. Prolongation of the PR interval
b. Prolongation of the QRS interval
c. Prolongation of the QT interval
d. All of the above
2. A block in the left bundle branch is most likely to cause which of the following?
a. Shortening of the PR interval
b. Prolongation of the QRS interval (duration)
c. Shortening of the QT interval
d. All of the above
3. Name four factors that may prolong the QT/QTc interval.
4. Which of the following events is/are never observed on a clinical 12-lead ECG?
a. Atrial depolarization
b. Atrial repolarization
c. His bundle depolarization
d. Ventricular depolarization
e. Ventricular repolarization
5. For this lead V1 recording, answer the following:

a. What is the heart rate?
b. How would you describe the component waves of this QRS over the phone?
c. What is the QRS duration?

Chapter 3: Answers
1. a. Prolong the PR interval.
2. b. Prolong the QRS interval (duration or width)
3. Drugs (such as ibutilide, sotalol, quinidine, procainamide, amiodarone), electrolyte abnormalities (hypocalcemia, hypokalemia), systemic hypothermia, evolving myocardial infarction with T wave inversions, etc. See Chapter 25 for a more extensive, but still not exhaustive list.
4. c. Depolarization of the His bundle is never seen on the surface ECG. This low-amplitude, high-frequency physiologic event occurs during the isoelectric part of the PR interval. His bundle activation, however, may be detectable using a special electrode system inside the heart during cardiac electrophysiologic (EP) procedures. (See Supplemental Extras, Intracardiac Recording.)
Note: Evidence of atrial repolarization is usually not seen on the standard ECG, but its signature may become apparent with acute pericarditis, in which there is often PR segment elevation in lead aVR (corresponding to the ST segment of the P wave) and PR segment depression in the inferolateral leads (see Chapter 12). In addition, sometimes with sinus rhythm and complete heart block, atrial repolarization (the atrial ST segment and atrial T wave) may be seen (unobscured by the QRS), appearing as low amplitude and short duration deflections of the baseline occurring just after each P wave.
5.
a. 100/min
b. RSR′ (communicated by phone or in person as “RSR-prime”) complex
c. About 130 to 140 msec (0.13-0.14 sec), which is abnormally wide, due in this case to right bundle branch block (Chapter 8). In addition, left atrial abnormality is present (Chapter 7), evidenced by a biphasic P wave in lead V1 with a prominent (at least 40 msec in duration) terminal component.

Chapter 4: ECG Leads

Review
The electrical currents produced during atrial and ventricular depolarization and repolarization are detected by electrodes placed on the extremities and chest wall.
Twelve leads are usually recorded in standard clinical electrocardiograms (ECGs):

1. The six limb (extremity) leads record voltages (electrical potentials) generated by the heart that are directed onto the frontal plane of the body. (This plane divides the body into front and back halves.) The six limb leads include three standard (bipolar) extremity leads (I, II, and III) and three augmented (unipolar) extremity leads (aVR, aVL, and aVF).
a. A standard bipolar lead records the difference between voltages from the heart detected at two extremities. The standard limb leads can be represented by Einthoven’s triangle. These three leads are related by the simple equation:
image
A unipolar lead records voltages at one point relative to an electrode with close to zero potential. The unipolar limb leads can also be represented by a triaxial diagram. They are related by the simple equation:
b. The three standard limb leads and the three augmented limb leads can be mapped on the same diagram such that the axes of all six leads intersect at a common point, producing the familiar hexaxial lead diagram.
c. As a general rule, the P-QRS-T pattern in lead I resembles that in lead aVL. Leads aVR and II usually show reverse patterns. The ECG patterns in lead aVF usually resemble those in lead III.
2. The six chest (precordial) leads (V1 to V6) record voltages generated by the heart and directed onto the horizontal (transverse) plane of the body (dividing the body into an upper and a lower half). These leads are obtained by means of electrodes placed in specific anatomic locations across the anterior-lateral chest wall.

In addition to the 12 conventional leads, ECGs can be recorded in special ways. For example, monitor leads, in which electrodes are placed on the anterior chest and sometimes abdominal wall, are employed in cardiac and intensive care units (CCUs and ICUs). Continuous ECGs can be recorded with the classical Holter apparatus for a period of 24 hours or more in ambulatory patients who are suspected of having intermittent events not captured on the standard 12-lead ECG, or to assess the heart rate (e.g., in sinus rhythm or in atrial fibrillation) during daily activities or during sleep. Very sporadic symptoms are better correlated with ECG rhythm changes by using one of a variety of the available external event recorders for periods of up to 2 to 4 or more weeks or longer. Increasingly, commercial “wearable” devices are being marketed directly to the consumer for self-monitoring or physician-assisted analysis. Standard Holter monitors are being largely replaced by cardiac event recorders capable of ECG rhythm monitoring for extended time periods (weeks to months). These longer time periods are often needed to correlate with transient symptoms and also with transient asymptomatic arrhythmias (e.g., atrial fibrillation, ventricular tachycardia, or AV heart block) that can be detected with reasonable reliability (and then reviewed by qualified readers) by automated programs.

Chapter 4: Questions
1. Leads I and II are shown here. Draw the P-QRS-T pattern in lead III.

2. Leads I, II, and III are shown here. What is “wrong” with their labeling?

3. Sketch the hexaxial lead diagram that shows the six frontal plane (limb) leads.
4. Why does the P-QRS-T pattern in lead aVR usually show a reverse of the pattern seen in lead II?

Chapter 4: Answers
1. Lead II = lead I + lead III. Therefore, by rearranging Einthoven’s lead equation, lead III = lead II − lead I as shown here. This equation means that the voltages of the P wave, QRS complex, and T wave in lead II should be equal to the sum of the P, QRS, and T voltages, in leads I and III, respectively, when measured at corresponding times.

2. The voltages in lead II do not equal those in leads I and III, thus apparently violating Einthoven’s lead equation. The reason is that leads II and III were mislabeled. When you reverse the labels, the voltage in lead II equals the voltages in leads I and III.

3.

4. The positive poles of leads aVR and lead II point in the opposite directions (150° apart), so the recorded P-QRS-T complexes will be nearly reversed images of each other: what is positive (upward) in one lead should be negative in the other, and vice versa

Chapter 5: The Normal ECG

Review
The three basic “laws” of electrocardiography are as follows:

1. A positive (upward) deflection is seen in any lead if the depolarization wave spreads toward the positive pole of that lead.
2. A negative (downward) deflection is seen if the depolarization wave spreads toward the negative pole (or away from the positive pole) of any lead.
3. If the mean orientation of the depolarization path is directed at right angles (perpendicular) to any lead, a biphasic (RS or QR) deflection is seen.

Atrial depolarization starts in sinus node and spreads from left to right and downward (toward the AV node), toward the positive pole of lead II and away from the positive pole of lead aVR. Therefore, with normal sinus rhythm the P wave is always positive in lead II and negative in lead aVR.
Ventricular depolarization normally comprises two major, sequential phases:

1. The first phase is stimulation of the ventricular septum. The vector is directed in an anterior and rightward direction. This initial phase of ventricular activation, therefore, accounts for the physiologic small (septal) r wave observed in the right chest leads (e.g., V1 and V2) and the small (septal) q wave seen in the left chest leads (e.g., V5 and V6).
2. During the second and major phase of ventricular depolarization, the stimulus spreads simultaneously outward (from endocardium to epicardium) through the right and left ventricles. Because the mass of the left ventricle normally overbalances that of the right ventricle, the spread of depolarization through the left ventricle predominates on the normal electrocardiogram (ECG). This vectorial “shift to the left” produces a relatively tall R wave in the left chest leads (e.g., V5 and V6) after the small “septal” q wave. In right chest leads (V1 and V2), the same process of ventricular stimulation produces a relatively deep S wave after the small initial (“septal”) r wave.

Chest leads between these extreme positions show a relative increase in R wave amplitude and a decrease in S wave amplitude, referred to as normal R wave progression.
In the extremity (limb) leads the morphology of the QRS complex varies with the so-called electrical position (axis) of the heart. These still useful terms from the classic ECG literature are descriptive rather than anatomical.

1. When the heart vector is said to be “electrically horizontal,” leads I and aVL show a qR pattern.
2. When the heart vector is said to be “electrically vertical,” leads II, III, and aVF show a qR pattern.

The normal T wave vector generally follows the direction of the main deflection of the QRS complex in any lead. In the chest leads the T wave may normally be negative in leads V1 and V2. In most adults the T wave becomes positive by lead V2 and remains positive in the left chest leads. In the extremity leads the T wave is always positive in lead II and negative in lead aVR. When the heart is “electrically horizontal,” the QRS complex and T wave are positive in leads I and aVL. When the heart is “electrically vertical,” the QRS complex and T wave are positive in leads II, III, and aVF.

Chapter 5: Questions
1. Examine the 12-lead ECG and lead II rhythm strip shown in the following figure. Then answer these questions:

a. Is sinus rhythm present?
b. In the extremity leads, does the QRS axis in the frontal plane have an electrically “vertical” or “horizontal” orientation?
c. With respect to the chest (horizontal plane) leads, where is the transition zone located?
d. Is the PR interval normal within normal limits?
e. Is the QRS interval (duration) within normal limits?
f. Are the T waves in the chest leads normal in appearance?

2. On the following ECG, is sinus rhythm present?

Chapter 5: Answers
1.
a. Yes. The P waves are positive (upright) in lead II and negative in lead aVR, with a rate of about 75 beats/min.
b. Electrically “vertical.” The R waves are most prominent in leads II, III, and aVF.
c. The transition zone is in lead V3. Note that the RS complexes have an R wave approximately equal to the S wave in this lead.
d. The PR interval is about 160 msec (0.16 sec). This is within the normal range (120-200 msec).
e. The QRS width is about 80 msec (= 0.08 sec; two small box widths). This is within normal limits (less than or equal to 100-110 msec).
f. Yes
2. No. Although a P wave appears before each QRS complex, the P wave is negative in lead II. With sinus rhythm, the P wave will always be positive (upright) in lead II, given the normal orientation of atrial depolarization forces from left to right and downward. Thus, in this patient, based on the P wave polarity, we can infer that the heart’s intrinsic pacemaker must be outside the sinus node (i.e., ectopic), probably in a low atrial focus near the atrioventricular (AV) junction. Inverted P waves in lead II such as these are sometimes called retrograde P waves because they indicate that the atria are depolarized in the opposite direction from normal, that is, from the bottom to the top rather than from the top (sinus node) to the bottom (AV junction); see also Chapters 13 and 14.

Chapter 6: Electrical Axis and Axis Deviation

Review
The term mean QRS axis describes the overall direction in which the QRS axis is oriented with respect to the frontal plane of the body. Therefore, the mean QRS axis is measured in reference to the six limb (frontal plane) leads. These leads can be arranged in the form of a hexaxial (six axes) diagram.
The mean QRS axis can usually be approximated by using one of the following rules:

1. The axis will be pointed midway between the positive poles of any two leads that show R waves of equal height.
2. The axis will be pointed at right angles (perpendicular) to any lead that shows a biphasic complex and toward other leads that show relatively tall R waves.

The normal mean QRS axis in adults lies between about −30° and +90 to +100°. An axis more negative than −30° is defined as left axis deviation (LAD). An axis more positive than +90 to 100° is defined as right axis deviation (RAD). Conceptually, LAD can be viewed as an extreme form of a horizontal electrical axis; RAD as an extreme form of a vertical electrical axis.

1. LAD can be readily recognized if lead II shows an RS complex in which the S wave is deeper than the R wave is tall. In addition, lead I will show a tall R wave and lead III a deep S wave. LAD is always seen in the electrocardiograms (ECGs) of patients with left anterior fascicular block (hemiblock) and may be seen in certain other pathologic conditions, such as left ventricular hypertrophy and inferior Q wave wall myocardial infarction. Sometimes it is seen in the ECGs of apparently healthy people.
2. RAD is present if the R wave in lead III is taller than the R wave in lead II. In addition, lead I shows an rS complex. RAD can be seen in several conditions, including left–right arms lead reversal; right ventricular overload syndromes, lateral wall myocardial infarction, chronic lung disease, and left posterior fascicular block (hemiblock) (see Chapter 25). In addition, RAD may be seen in the ECGs of normal people (especially younger adults and is the normal finding in neonates). It also occurs with dextrocardia.

More rarely the QRS complex is biphasic in all six limb leads. This makes the mean electrical axis indeterminate, but this finding is not associated with any specific abnormality.
The mean electrical axis of the P wave and T wave can be estimated in the same manner as the mean QRS axis. With sinus rhythm, the normal P wave is about +60° (positive P wave in lead II). Normally the T wave axis in the frontal plane is similar to the QRS axis. Therefore, the T waves normally are positive in leads with a predominantly positive QRS complex.

Chapter 6: Questions
1. Based on the six limb leads (I, II, III, aVR, aVL, and aVF) shown here, what is the approximate mean QRS axis?

2. Tracings (A), (B), and (C) are, in mixed order, leads I, II, and III from an ECG with a mean QRS axis of −30°. This information should allow you to sort out which lead is which.

3. All but which ONE of the following conditions may cause right axis deviation?

a. Reversal of left and right arm electrodes
b. Severe chronic obstructive pulmonary disease
c. Lateral wall myocardial infarction
d. Acute or chronic pulmonary embolism
e. Left anterior fascicular block (hemiblock)

4. What is the mean electrical axis here? ECG shows sinus tachycardia, PR = 190 msec and prominent P waves.

Chapter 6: Answers
1. The (mean, frontal plane) QRS axis is roughly +60°. Notice that the QRS complex in lead aVL is biphasic. Therefore, the mean QRS axis must point at a right angle to −30°. In this case the axis is about +60° because leads II, III, and aVF are positive. Note that the R wave in lead III is slightly taller than the R wave in lead I. If the axis were exactly +60°, these waves would be equally tall. Thus, the axis must be somewhat more positive than +60°, probably around +70°. Estimating the QRS axis to within 10° to 20° is usually quite adequate for clinical diagnosis. (Einthoven’s triangle and the hexaxial lead diagram are not precise representations of the lead relationships. Furthermore, different methods for calculating the mean frontal plane axis with the framework (based on waveform amplitudes, areas, vector analysis, etc. will yield slightly different values).
2. (A) lead II; (B) lead I; (C) lead III. Explanation: If the mean QRS axis is about −30°, the QRS axis will be pointed toward the positive pole of lead I (which is at 0°) and away from the positive pole of lead III (which is at +120°). Thus, lead I must be (B) and lead III must be (C). Lead II is (A) since the mean axis at girth angles to this lead axis. The positive pole of lead II is at +60° on the hexaxial diagram. If the mean QRS axis is about −30°, lead II must show a biphasic complex because the mean QRS axis is at right angles to that lead.
3. Left anterior fascicular (hemi-) block is associated with marked left axis deviation (formally defined as ≥45°).
4. Note the relatively tall R waves in the inferior leads, with R wave amplitude in lead III > R in lead II. Right axis deviation here was associated with a major clinical abnormality, namely right ventricular hypertrophy (RVH). Note also the slightly peaked P waves in lead II, which are of borderline amplitude for right atrial overload (see Chapter 7). The biphasic QRS in aVR with equal Q and R waves indicates that the mean QRS axis is directed at right angles to the aVR lead axis, i.e., at −60° or +120°. Since lead II shows a positive (R) wave, the QRS axis here is about +120°.

Chapter 7: Atrial and Ventricular Enlargement

Review
When cardiac enlargement occurs, the total number of heart muscle fibers does not increase; rather, each individual fiber becomes larger (hypertrophied). With dilation, the heart muscle cells become longer (termed eccentric hypertrophy). With enlargement due to of increased wall thickness, the cells become wider (termed concentric hypertrophy). One predictable electrocardiogram (ECG) effect of cardiac hypertrophy is an increase in the voltage or duration of the P wave or of the QRS complex. Increased wall thickness and chamber dilation occur together. Chamber enlargement usually results from some type of chronic pressure or volume load on the heart muscle. Other causes of hypertrophy relate to genomic mutations, exemplified by hereditable hypertrophic cardiomyopathies.
Pathologic hypertrophic syndromes are often accompanied by fibrosis (scarring) and changes in myocardial geometry (remodeling), which may both worsen myocardial function and promote arrhythmogenesis (e.g., atrial fibrillation and sustained ventricular tachycardia).
Right atrial abnormality (RAA), or right atrial overload, may be associated with tall, peaked P waves exceeding 2.5 mm in height. These waves are usually best seen in leads II, III, aVF, and sometimes V1 or V2.
Left atrial abnormality (LAA), with or without frank left atrial enlargement, is manifested by wide, sometimes notched P waves of 0.12 sec or more duration in one or more of the extremity leads. A biphasic P wave with a prominent wide negative deflection may be seen in lead V1. A more contemporary and increasingly used diagnostic label, inferable from very broad P waves (>120 msec) with a distinctive morphology, is interatrial conduction delay (IACD). The most advanced manifestation of IACD is a broad, notched sinus P wave in lead II (and often III and aVF) that is initially positive and then negative. These abnormal P waves have been associated increased risk of atrial fibrillation.
The ECG diagnosis of biatrial abnormality (enlargement) is based on the presence of tall and broad P waves. Such prominent P waves may be a clue to severe valvular disease or cardiomyopathy.
Right ventricular hypertrophy, especially due to chronic pressure overload syndromes, may produce any or all of the following:

1. A tall R wave in lead V1, equal to or larger than the S wave in that lead
2. Right axis deviation
3. T wave inversions in the right to middle chest leads (sometimes called a right ventricular “strain” pattern)

With left ventricular hypertrophy (LVH), any or all of the following may occur:

1. The sum of the depth of the S wave in lead V1 (SV1) and the height of the R wave in either lead V5 or V6 (RV5 or RV6) exceeds 35 mm (3.5 mV), especially in middle-aged or older adults. However, high voltage in the chest leads is a common normal finding, particularly in athletic or thin young adults. Consequently, high voltage in the chest leads (SV1 + RV5 or RV6 >35 mm) is not a specific LVH indicator.
2. Another proposed set of LVH criteria (the Cornell voltage indexes) are based by summing components of the QRS voltages in leads V3 and aVL: for men, SV3 + RaVL >28 mm; for women, SV3 + RaVL >20 mm.
3. Sometimes LVH produces tall R waves in lead aVL. An R wave of 11 to 13 mm (1.1-1.3 mV) or more in lead aVL is another sign of LVH. A tall R wave in lead aVL may be the only ECG sign of LVH, and the voltage in the chest leads may be normal. In other cases the chest voltages are abnormally high, with a normal R wave seen in lead aVL.
4. Just as RVH is sometimes associated with repolarization abnormalities due to ventricular overload, so ST-T changes are often seen in LVH. This LV overload-related repolarization abnormality (formerly called LV “strain”) is usually best seen in leads with tall R waves.
5. With LVH the mean QRS electrical axis is usually horizontal (i.e., in the direction of lead I). Actual left axis deviation (i.e., an axis −30° or more negative) may also be seen. In addition, the QRS complex may become wider. Not uncommonly, patients with LVH eventually develop an incomplete or complete left bundle branch block (LBBB) pattern. LVH is a common cause of an intraventricular conduction delay (IVCD) with features of LBBB.
6. Signs of LAA (broad P waves in the extremity leads or biphasic P waves in lead V1, with a prominent negative, terminal wave) are often seen in patients with ECG evidence of LVH. Most conditions that lead to LVH ultimately produce left atrial overload as well.

The diagnosis of LVH should not be made solely on the basis of high voltage in the chest leads because high voltages may occur normally, particularly in young adults, athletes, and lean individuals (exemplifying the limited specificity of voltage criteria; see Chapter 24). In addition, enlargement of any of the four cardiac chambers can be present without diagnostic ECG changes (exemplifying the limitation of sensitivity). Echocardiography is considerably more sensitive and specific than ECG analysis in assessing chamber enlargement.

Chapter 7: Questions
1. Examine the following ECG from a 72-year-old man:

a. What is the heart rate?
b. Name at least two abnormal findings.
2. True or false: Echocardiography is more sensitive and specific than the ECG in assessing chamber enlargement. (However, the ECG may show abnormalities of interatrial conduction, based on low amplitude notching or P wave prolongation, which are not apparent from the echocardiogram.)

Chapter 7: Answers
1.
a. About 100 beats/min
b. Note that the P waves, coming just before the QRS complexes, are negative in II and positive in aVR, indicating an AV junctional or low ectopic atrial rhythm. LVH voltage criteria are met and there are nonspecific ST-T changes in the inferolateral leads that could be due to LVH, ischemia, etc.
2. True

Chapter 8: Ventricular Conduction Disturbances: Bundle Branch Blocks and Related Abnormalities

Review
Right bundle branch block (RBBB) produces the following characteristic patterns: an rSR′ with a prominent wide final R’ wave in lead V1, a qRS with a wide, terminal S wave in lead V6, and a QRS width of 120 msec (three small time boxes) or more. Incomplete RBBB shows the same chest lead patterns, but the QRS width is between 100 and 120 msec.
Left bundle branch block (LBBB) produces the following characteristic patterns: deep wide QS complex (or occasionally an rS complex with a wide S wave) in lead V1, a prominent (often notched) R wave without a preceding q wave in lead V6, and a QRS width of 120 msec or more. Incomplete LBBB shows the same chest lead patterns as LBBB, but the QRS width is between 100 and 120 msec.
Fascicular blocks (hemiblocks) can occur because the left bundle splits into two main subdivisions (fascicles): the left anterior fascicle and the left posterior fascicle. Conduction through either or both of these fascicular subdivisions can be blocked.
Left anterior fascicular block or hemiblock is characterized by a mean QRS axis of about −45° or more. (When the mean QRS axis is about −45°, left axis deviation is present and the height of the R wave in lead I [RI] is equal to the depth of the S wave in lead aVF [SaVF]. When the mean QRS axis is more negative than about −45°, SaVF becomes larger than RI.)
Left posterior fascicular block or hemiblock is characterized by marked right axis deviation (RAD). However, before the diagnosis of left posterior fascicular block is made, other more common causes of RAD must be excluded, including lead reversal (left/right arm electrodes), normal variants, right ventricular overload syndromes (including chronic lung disease), and lateral wall infarction (see Chapter 25).
“Bifascicular block” patterns indicate blockage of any two of the three fascicles. For example, RBBB with left anterior fascicular block (LAFB) produces an RBBB pattern with marked LAD. RBBB with left posterior fascicular block produces an RBBB pattern with RAD (provided other causes of RAD, especially right ventricular hypertrophy and lateral myocardial infarction, are excluded). Similarly, a complete LBBB may indicate blockage of both the anterior and posterior fascicles.
Bifascicular block patterns are potentially significant because they make ventricular conduction dependent on the single remaining fascicle. Additional damage to this third remaining fascicle may completely block AV conduction, producing complete heart block (trifascicular block). The term “trifascicular block,” however, is rarely used in clinical practice. Occasionally one can infer trifascicular block from a 12-lead electrocardiogram (ECG), without sustained or intermittent complete or advanced AV block, when patients display alternating bundle branch block (RBBB and LBBB), thus placing them at high risk of abrupt complete AV heart block.
Caution: a very common misconception is that bifascicular block patterns (especially RBBB and LAFB) in concert with a prolonged PR interval are diagnostic of trifascicular disease. This inference is often wrong because the long PR interval may represent a delay in the AV node, not in the infranodal part of the conduction system
The acute development of new bifascicular block, usually RBBB and LAFB (especially with a prolonged PR interval), during an acute anterior wall myocardial infarction (Chapters 9 and 10), may be an important warning signal of impending complete heart block and is considered by some a strong indication for a temporary pacemaker. However, chronic bifascicular blocks with normal sinus rhythm have a low rate of progression to complete heart block and are not indications by themselves for permanent pacemakers.

Chapter 8: Questions
1. Examine the chest leads shown here and then answer these questions:
a. What is the approximate QRS width?
b. What conduction disturbance is present?
c. Why are the T waves in leads V1 to V3 inverted?
2. Examine carefully the 12-lead ECG and lead II rhythm strip shown below. Can you identify the major conduction abnormality?

3. Define the terms primary and secondary T wave abnormality.

True or false (Questions 5 to 8):

4. Left anterior fascicular block (hemiblock) does not markedly widen the QRS complex.
5. Left bundle branch block is usually a biomarker of organic (structural) heart disease.
6. Bundle branch blocks may occur transiently.
7. What type of conduction disturbance does the above ECG show?
8. An electronic pacemaker stimulating the left ventricle will produce a left bundle branch block pattern.
9. What type of conduction disturbance does the ECG below show?

10. What is the rhythm? What conduction disturbance is present.

Chapter 8: Answers
1.

2.

a. 120 msec
b. Right bundle branch block
c. Secondary T wave inversions may be seen in the right chest leads with right bundle branch block (see text and answer to Question 4).

3. Left bundle branch block. The PR interval is also prolonged (240 msec) because of a delay in AV conduction (first-degree AV block or delay).
4. Primary T wave abnormalities result from actual changes in ventricular repolarization caused, for example, by drugs, ischemia, or electrolyte abnormalities. These abnormalities are independent of changes in the QRS complex. Secondary T wave changes, by contrast, are related entirely to alterations in the timing of ventricular depolarization as observed in conditions in which the QRS complex is abnormally widened. For example, with bundle branch block a change in the sequence of depolarization also alters the sequence of repolarization, causing the T wave to point in a direction opposite the last deflection of the QRS complex. Thus, with right bundle branch block the T waves are secondarily inverted in leads with an rSR’ configuration (e.g., V1, V2, and sometimes V3) because of a delay in right ventricular repolarization. With left bundle branch block the secondary T wave inversions are seen in leads with tall, wide R waves (V5 and V6) due to a delay in left ventricular repolarization. Secondary T wave inversions are also seen with ventricular paced beats and Wolff–Parkinson–White (WPW) preexcitation patterns (Chapter 18). Sometimes, primary and secondary T wave changes are seen on the same ECG, as when ischemia develops in a patient with a bundle branch block. In such cases, the ECG might show prominent T wave inversions or ST depressions in leads V1-V3 (with QS or rS waves), not the expected ST elevations and relatively tall positive T waves.
5. True
6. True
7. True
8. False. It should produce an RBBB pattern because the left ventricle is stimulated before the right.
9. Complete RBBB. Rhythm is sinus tachycardia at rest (100/min). The QRS axis is leftward, but strict criteria for left axis deviation (−30°) and certainly for left anterior fascicular block (−45°) are not met. The P waves are somewhat prominent with a broad negative component, suggesting left atrial abnormality (see Chapter 7). The PR interval is normal. Leads V1 and V2 show classic rsR′ patterns with negative T waves. The latter are consistent with repolarization abnormalities secondary to RBBB. Finally, note that the notching at the end of the QRS in leads V4 to V6 is actually an S wave, not an inverted P wave. These small deflections lie within the span of the prolonged QRS duration (about 130 msec) as measured at their widest interval.
10. Rhythm is sinus at a rate of about 80 beats/min. Classic example of complete left bundle branch block (LBBB). Note the wide QRS complexes in lead V1 and the wide, notched R waves in leads V4 to V6 (“M-shape” in V4). The ST depressions and T wave inversions (secondary repolarization abnormalities) in leads with predominant R waves are also characteristic of LBBB, as are the slight J point/ST elevations in leads V1 to V3.

Chapter 9: Myocardial Infarction and Ischemia, Part I: ST Segment Elevation and Q Wave Syndromes

Review
Myocardial ischemia occurs when the blood supply to the myocardium is not adequate. Myocardial infarction (MI) refers to necrosis of the myocardium caused by severe ischemia. Myocardial ischemia or infarction may affect the entire thickness of the ventricular muscle (transmural injury) or may be localized to the inner layer of the ventricle (subendocardial ischemia or infarction). Transmural (or nearly transmural) MI, especially when large, often (but not always) produces a typical sequence of ST-T changes and often abnormal Q waves. The ST-T changes can be divided into two phases:

1. The acute phase of ST segment elevation MI (STEMI), sometimes also referred to as transmural MI/ischemia, is marked by ST segment elevations (current of injury pattern) and sometimes by relatively tall positive T waves (hyperacute T waves).
2. The evolving phase is characterized by the appearance of inverted T waves, usually most apparent in leads that showed the hyperacute T waves and ST segment elevations.

These ST-T changes occur during a period of hours or days and usually resolve over weeks or months. During the first day or so after an MI, new abnormal Q waves may appear in one or more leads. Pathologic Q waves are more likely in the evolution of larger ST-elevation infarcts.
Recognition of STEMI is vital because this diagnosis is the major indication for emergency reperfusion, preferably with a percutaneous coronary intervention. The sooner the “culprit” artery is reperfused, the better the clinical outcome. Prompt percutaneous coronary intervention (PCI) therapy (e.g., within 24 hours) may also be helpful in the treatment of selected patients with non-STEMI.
The persistence of ST segment elevations for more than 2 or 3 weeks after an acute MI may signify that a ventricular aneurysm has developed. The abnormal Q waves tend to persist but may become smaller with time and rarely may even disappear.
An ST elevation/Q wave MI can also be described in terms of its electrocardiogram (ECG) location. With an anterior infarction, ST segment elevations and abnormal Q waves occur in one or more of leads V1 to V6, I, and aVL. Reciprocal ST depressions may be seen in leads II, III, and aVF. With an inferior infarction, ST elevations and Q waves appear in leads II, III, and aVF, and reciprocal ST depressions may be seen in one or more of the anterior leads. Not all STEMIs are accompanied by reciprocal changes.
Acute right ventricular MI is a common complication of inferoposterior infarcts. ECG diagnosis is based on the presence of elevated ST segments in the right chest leads (e.g., V3R, V4R).
To be emphasized: the clinical equation of pathologic Q waves with transmural necrosis is an oversimplification. Not all transmural infarcts lead to Q waves, and not all Q wave infarcts correlate with transmural infarction.
The pathologic Q waves of infarction must also be distinguished from normal Q waves. For example, small normal septal q waves as part of qR complexes may be seen in the left chest leads (V4 to V6), in leads II, III, and aVF (with a vertical electrical axis), and in leads I and aVL (with a horizontal axis). These septal q waves are normally less than 40 msec in width.
A QS wave may be seen normally in lead V1 and occasionally in leads V1 and V2. Q waves may also be seen as normal variants in leads aVF, III, and aVL.
Multiple MIs can occur. In such cases the ECG shows old Q waves from the preceding infarct and new Q waves with ST-T changes from the current infarct.
When RBBB complicates an acute MI, the diagnosis of both conditions is possible. The RBBB prolongs the QRS width, and lead V1 shows a tall, positive final deflection. In addition, abnormal Q waves and ST segment elevations resulting from the acute MI are present in the chest leads with an anterior MI and in leads II, III, and aVF with an inferior MI.
When LBBB complicates an acute MI, the infarction may be difficult to diagnose because the LBBB may mask both the abnormal Q waves of the infarction and the ST segment elevations and T wave inversions of the ischemia. In addition, LBBB may produce QS waves in the right chest leads with ST segment elevations and slow R wave progression across the chest without MI. The presence of QR complexes in the left chest leads with LBBB is suggestive of underlying MI with scar/fibrosis formation. Ischemia (acute or evolving) with underlying LBBB is suggested by the presence of T wave inversions in the right chest leads, ST segment elevations in the left chest leads (or in other leads with prominent R waves), or ST segment depressions in the right precordial leads (or other leads with rS or QS waves).

Chapter 9: Questions and Answers
See the end of Chapter 10.

Chapter 10: Myocardial Infarction and Ischemia, Part II: Non-ST Segment Elevation and Non-Q Wave Syndromes

Review
Subendocardial ischemia generally produces ST segment depressions, which may appear only in the anterior leads (I, aVL, and V1 to V6), only in the inferior leads (II, III, and aVF), or diffusely in both groups of leads. (The combination of diffuse ST depressions, especially in conjunction with with prominent ST elevation in lead aVR may be caused by left main coronary disease or severe three-vessel coronary disease.)
These ischemic ST segment depressions may be seen during attacks of typical angina pectoris or of “anginal equivalents,” such as dyspnea or left arm pain. Similar ST segment depressions may develop during exercise (with or without chest pain) in patients with ischemic heart disease. The presence of ischemic heart disease may be determined by recording the electrocardiogram (ECG) during exercise (stress electrocardiography). ST segment depression of 1 mm or more, lasting 80 msec or more, is generally considered a positive (abnormal) response. However, false-negative (normal) results can occur in patients with ischemic heart disease, and false-positive results can occur in normal people.
Ischemic ST segment changes may also be detected during ambulatory ECG (Holter) monitoring. Analysis of these records has shown that many episodes of myocardial ischemia are not associated with angina pectoris (silent ischemia).
With non-Q wave infarction the ECG may show persistent ST segment depressions or T wave inversions. Abnormal Q waves do not usually occur with subendocardial infarction limited to roughly the inner half of the ventricular wall. Acute ischemia due to left main coronary obstruction or severe three-vessel disease may present with both changes: ST depressions in most of the anterior and inferior leads, with ST elevations in lead aVR and sometimes V1.
With Prinzmetal’s angina, transient ST segment elevations suggestive of epicardial or transmural ischemia occur during attacks of angina. Patients with Prinzmetal’s angina often have atypical chest pain since it occurs at rest or at night. In contrast, patients with classic angina typically have exertional pain that is associated with ST segment depressions. Prinzmetal’s (variant) angina pattern is generally a marker of coronary artery spasm with or without underlying coronary obstruction.
The ST segment elevations of acute transmural MI can be simulated not only by the Prinzmetal’s angina but also by the normal variant ST elevations seen in healthy people (physiologic early repolarization pattern), with acute pericarditis (see Chapter 11), with the Brugada pattern (Chapter 21), and with a number of other conditions summarized in Chapter 25.
Another distinct, non-atherosclerotic syndrome is referred to by various terms, especially acute stress or takotsubo cardiomyopathy (also called left ventricular apical ballooning syndrome). Most patients are middle-aged to older women who present with chest pain and ECG changes (ST elevations or depressions, or T wave inversions) and elevated serum cardiac enzyme levels mimicking the findings of a classic acute or evolving MI due to coronary occlusion. Imaging studies (echocardiographic and angiographic) may show left ventricular apical akinesis or dyskinesis (absence of contraction or outward “ballooning”). However, epicardial coronary disease is not present. Instead, the pathophysiology may be related to coronary vasospasm and/or myocardial damage mediated by neurogenic and neurohumoral factors increasing myocardial oxygen demands in the context of emotional or physical stress.
The abnormal ST depressions of subendocardial ischemia may be simulated by the repolarization abnormalities of left ventricular hypertrophy, digoxin effect (see Chapter 20), or hypokalemia (see Chapter 11), as well as other conditions summarized in Chapter 25.
T wave inversions can be a sign of ischemia or infarction, but they may also occur in a variety of other settings (see Chapter 25), such as in normal variants or with ventricular hypertrophy, subarachnoid hemorrhage, after ventricular pacing or transient LBBB (“memory” T wave syndrome” (see Online Section 2), and with secondary ST-T changes associated with bundle branch blocks (Chapter 8).

Chapters 9 and 10: Questions
1. Answer these questions about the following ECG:

a. What is the approximate heart rate?
b. Are ST segment elevations present?
c. Are abnormal Q waves present?
d. What is the diagnosis?
2. Answer these questions about the following ECG:

a. What is the approximate mean QRS axis?
b. Is the R wave progression in the chest leads normal?
c. Are the T waves normal?
d. What is the diagnosis?

3. Complete this statement: Persistent ST segment elevations (often with pathologic Q waves) several weeks or more after an infarction may be a sign of ______________, which should be apparent on an echocardiogram.
4. What ECG abnormality is shown here, and what symptom might this patient be presenting with?

5. What conduction disturbance is present in the ECG below? What other major abnormality is present?

6. True or false: Acute (emergency) percutaneous intervention with an angioplasty-type procedure or thrombolysis therapy has been found to be equally effective for ST segment elevation MI and non-ST segment elevation MI.
7. The ECG below is consistent with which ONE of the following conditions?

a. Right coronary artery occlusion
b. Left circumflex coronary artery occlusion
c. Left anterior descending coronary artery occlusion
d. Left bundle branch block
e. Left main coronary artery occlusion

Chapters 9 and 10: Answers
1.
a. 100 beats/min
b. Yes. In leads II, III, and aVF, with reciprocal ST depressions in leads V2 to V4, I, and aVL.
c. Yes. Best seen in leads III and aVF.
d. Acute inferior wall infarction
2.
a. About +90°. Between +80° and 90° is acceptable.
b. No
c. No. Notice the inverted T waves in leads V2 to V6, I, and aVL.
d. Anterior wall infarction, possibly recent or evolving
3. Left ventricular aneurysm (large akinetic/dyskinetic zone)
4. Marked ST segment depressions. This patient had severe ischemic chest pain with a non-ST segment elevation/non-Q wave infarct.
5. The ECG shows a right bundle branch block pattern (RBBB) with an evolving anterior Q wave infarct. With “uncomplicated” RBBB the right chest leads show an rSR′ pattern. Note that leads V1, V2, and V3 show wide QR waves (120 msec) due to the anterior Q wave myocardial infarction and RBBB. The ST elevations in leads V1, V2, and V3 and the T wave inversions across the chest leads are consistent with recent or evolving myocardial infarction.
6. False. Acute (emergency) percutaneous coronary intervention (PCI) or thrombolytic therapy in the shortest possible timeframe has been demonstrated to have consistent benefit only in acute ST segment elevation MI (STEMI). Immediate revascularization (within 12-24 hours) may also be useful in selected patients with non-STEMI.
7. c. Anterior wall STEMI. The findings are consistent with acute occlusion of the proximal left anterior descending coronary artery.

Chapter 11: Drug Effects, Electrolyte Abnormalities, and Metabolic Disturbances

Review
The electrocardiogram (ECG) can be influenced by numerous factors, including many drugs and certain metabolic disturbances.
Digitalis effect refers to the characteristic scooped-out depression of the ST segment produced by therapeutic doses of digitalis. Digitalis toxicity refers to the arrhythmias and conduction disturbances produced by excessive doses of digitalis (see Chapter 20).
Many drugs, including quinidine, procainamide, disopyramide, ibutilide, dofetilide, sotalol, methadone, haloperidol, certain psychotropic drugs, and certain antibiotics, can prolong the QT interval and may induce a potentially lethal type of ventricular tachycardia called torsades de pointes (see Chapter 16). Patients likely to develop this complication usually show prominently prolonged QT (QTc) intervals and/or large U waves. Amiodarone is an antiarrhythmic drug that typically prolongs the QT interval, even at therapeutic doses (although it is less likely to cause torsades de pointes compared to other class 3 antiarrhythmics).
Lithium carbonate in toxic doses may cause sinus node dysfunction. Donepezil, rivastigmine and galantamine, which are vagotonic drugs used to treat Alzheimer’s disease, may cause prominent bradyarrhythmias, especially in concert with beta blockers.
Certain electrolyte disturbances can also affect the ECG:

1. Hyperkalemia typically produces a sequence of changes. Initially, the T wave narrows and peaks (“tents”). Further elevation of the serum potassium concentration usually leads to prolongation of the PR interval and then to loss of P waves and widening of the QRS complex, followed by a “sine wave” pattern and asystole, with cardiac arrest.
2. Hypokalemia may produce ST depressions and prominent U waves. The QT interval becomes prolonged. (In some cases you are actually measuring the QU interval, and not the QT interval; it may be impossible to tell where the T wave ends and the U wave begins.)
3. Hypercalcemia may shorten the QT interval, by abbreviating the ST segment, and hypocalcemia may prolong the QT interval, by “stretching out” the ST segment phase.
4. Hypomagnesemia and hypermagnesemia are important because they may be overlooked in clinical evaluation and may play a role in the genesis of ventricular arrhythmias and contribute to other metabolic disturbances. However, neither abnormality, in isolation, is associated with specific ECG alterations. Hypomagnesemia has been implicated in ventricular arrhythmogenesis with acute myocardial infarction and also in QT(U) prolongation syndromes with risk of torsades de pointes. Hypermagnesemia (usually due to renal failure or excessive intake) does not produce distinct ECG abnormalities when levels are only mildly or moderately elevated. Pronounced elevations may be associated with a prolonged PR or QRS interval. Extreme elevations, especially >15 to 20 mEq/L, may lead or contribute to cardiac arrest.

With systemic hypothermia the ECG often shows a humplike elevation (J wave or Osborn wave) located at the junction (J point) at the end of the QRS complex and the beginning of the ST segment. The pattern disappears with rewarming.
Thyroid disorders may also be associated with ECG changes. Severe hypothyroidism (myxedema) may lead to sinus bradycardia and low voltage (the latter due to pericardial effusion). In contrast, hyperthyroidism (due, for example, to Graves’ disease or excess thyroid replacement) may cause resting sinus tachycardia and, importantly, increases the risk of atrial fibrillation (Chapter 15).

Chapter 11: Questions
1. Which of the following factors can produce precordial ST segment elevations?
a. Hypokalemia
b. Early repolarization pattern (as normal variant)
c. Digitalis effect
d. Left ventricular aneurysm post MI
e. Hypocalcemia
f. Right bundle branch block
g. Acute pericarditis
2. Match ECGs (A), (B), and (C) with the following causes:

a. Digitalis effect
b. Hyperkalemia
c. Hypokalemia
3. Prominent U waves are most characteristic of which ONE of the following:
a. Hyperkalemia
b. Hypokalemia
c. Hyponatremia
d. Hypocalcemia
e. Digitalis effect

Chapter 11: Answers
1.
b. Normal variant early repolarization pattern
d. Left ventricular aneurysm
g. Acute pericarditis
2.
a. Digitalis effect (B)
b. Hyperkalemia (A)
c. Hypokalemia (C)
3.
b. Hypokalemia

Chapter 12: Pericardial, Myocardial, and Pulmonary Syndromes

Review
Acute pericarditis typically produces diffuse ST segment elevations, observable in multiple chest leads and also in leads I, aVL, II, and aVF. These ST elevations are attributable to a ventricular (epicardial) current of injury produced by the pericardial inflammatory process. Concomitant PR segment elevation in lead aVR with PR depression in the inferolateral leads may be caused by an atrial current of injury. Abnormal Q waves do not develop. After a variable period, the ST segment elevations may be followed by T wave inversions.
Large pericardial effusions are an important cause of low voltage of the QRS complexes (amplitudes of 5 mm or less in the six extremity leads). However, low voltage is not specific for pericardial effusion; it may also occur with obesity, anasarca, emphysema, myocarditis, and diffuse myocardial injury or infiltration (e.g., with amyloid), among other pathologic causes.
Pericardial effusion complicated by cardiac tamponade is often associated with sinus tachycardia and low QRS voltage complexes. Some patients also have electrical alternans, characterized by a periodic, beat-to-beat variation in the QRS appearance, producing an ABABAB-type pattern. Electrical alternans of this type is usually most apparent in the chest leads.
Unfortunately, no single electrocardiogram (ECG) pattern or constellation of findings is diagnostic of (chronic) constrictive pericarditis. Nonspecific ST-T wave changes and relatively low QRS voltages are most common. The PR/ST segment deviations may resemble those of acute pericarditis. However, atrial arrhythmias, especially atrial fibrillation, may preclude assessment of PR segment deviations.
Acute or chronic myocarditis can produce ST-T changes that are nonspecific or that resemble the changes of pericarditis or myocardial infarction (MI). It may also be associated with high-grade atrial or ventricular arrhythmias (e.g., atrial fibrillation or ventricular tachycardia). Myocarditis is a rare but important cause of sudden cardiac arrest/death (Chapter 21). Myocarditis may be caused by multiple factors, including viral infections (including COVID-19), parasitic infections, non-infectious inflammatory processes, and so forth. HIV/AIDs may be associated with ECG changes from a number of mechanisms, including myocarditis/cardiomyopathy, pericardial effusion, pulmonary hypertension, drug-related effects and toxicities (especially acquired long QT syndrome), and premature coronary atherosclerosis. Lyme disease (caused by B. burgdorferi spirochetal infection) may be associated with myocardial or pericardial involvement, but AV blocks are the most common manifestation of carditis in this syndrome.
The ECG may provide important clues to the etiology of chronic heart failure, including evidence of extensive MI, left ventricular hypertrophy from hypertension, diffusely low voltage from cardiac amyloid, and so forth. Patients with dilated cardiomyopathy from any cause may have a distinctive ECG pattern (the ECG-CHF triad):

1. Relatively low voltages in the extremity leads, such that the QRS in each of the six extremity leads is 8 mm or less in amplitude.
2. Relatively prominent QRS voltages in the chest leads, such that the sum of the S wave in either lead V1 or lead V2 plus the R wave in V5 or V6 is 35 mm or more.
3. Very slow R wave progression defined by a QS- or rS-type complex in leads V1 to V4.

Acute pulmonary embolism may produce any of the following patterns:

1. Sinus tachycardia as well as a variety of atrial/ventricular arrhythmias
2. T wave inversions V1 to V3 or V4 (RV “strain” pattern)
3. SIQIIITIII pattern
4. Rightward axis QRS shift
5. ST segment depressions resulting from subendocardial ischemia
6. Right bundle branch block (complete or incomplete) or QR in V1
7. Peaked P waves due to right atrial overload

Although most patients with acute pulmonary embolism have sinus tachycardia, no ECG finding is specific. Massive pulmonary embolism may also be associated with ST elevations in the right precordial leads, simulating acute ST elevation MI.
Patients with chronic thromboembolic pulmonary hypertension (CTEPH) due to recurrent pulmonary emboli may produce signs of right ventricular overload or frank RVH (tall R in V1, right axis deviation and right precordial T wave inversions), sometimes with peaked P waves caused by right atrial overload.
Severe chronic obstructive pulmonary disease (COPD) caused by emphysema often produces a relatively characteristic combination of ECG findings, including low QRS voltage, slow R wave progression in the chest leads, and a vertical or rightward QRS axis in the frontal plane. Peaked P waves (right atrial overload pattern) may also be present, with a vertical to rightward P wave axis.
A number of hereditary neuromuscular diseases are associated with major, sometimes life-threatening myocardial or conduction system involvement. The most common are Duchenne muscular dystrophy (X-linked recessive) and myotonic dystrophy, type 1 (autosomal dominant).

Chapter 12: Questions
1. Sinus tachycardia with electrical alternans is most indicative of which ONE of the following life-threatening conditions?
a. Pericardial effusion with cardiac tamponade
b. Acute myocardial infarction
c. Acute pulmonary embolism
d. Emphysema with respiratory failure
e. Acute viral myocarditis
2. True or false: The ECG is a highly sensitive and specific test for acute pulmonary embolism.
3. This ECG from a 36-year-old man with chest discomfort is most consistent with which ONE of the following diagnoses?
a. Acute pericarditis
b. Acute ST elevation MI (STEMI)
c. Brugada pattern
d. Normal variant (benign) early repolarization
e. Prinzmetal’s (vasospastic) angina

Chapter 12: Answers
1. a
2. False
3. a. The ECG shows sinus rhythm with normal intervals and normal QRS axis (about +60°). Note the diffuse, concave (spoon-shaped) ST elevations (except for lead aVR and V1), with discordant PR segment deviations (upward in lead aVR and downward in the inferolateral leads). The patient had acute idiopathic pericarditis.

Part II: Cardiac Rhythm Disturbances

Chapter 13: Sinus and Escape Rhythms

Review
With sinus rhythm, each heartbeat originates in the sinoatrial (SA) node. Therefore, the P wave is always negative in lead aVR and positive in lead II. The “normal sinus heart rate” (assuming 1:1 AV conduction) at rest or with modest activity is usually reported as between 50 to 60 and 100 beats/min. Slower rates are defined as sinus bradycardia and faster ones as sinus tachycardia. However, in healthy subjects, resting rates of about 50 to 80 beats/min are most common. Even slower rates at rest are observed, especially in endurance athletes. Sustained resting rates of 90 beats/min or more are nonspecific but raise consideration of anxiety, anticholinergic or sympathomimetic drug effects, hyperthyroidism, anemia, fever, lung disease, and so on. In patients with chronic heart failure, sinus tachycardia at rest may be an important sign of decompensation.
Usually subtle beat-to-beat variations in sinus rate are seen as a physiologic finding. The directional changes in rate are typically phasic with respiration (respiratory sinus arrhythmia), with increases during inspiration and decreases during expiration. SA node dysfunction (due to either pacemaker cell failure or exit block) may lead to sinus pauses or, in extreme cases, SA arrest. Prolonged sinus arrest causes fatal asystole unless normal sinus rhythm resumes or sustained escape beats originating in subsidiary pacemaker sites in the atria, atrioventricular junction, or ventricles supervene. SA dysfunction may be seen, particularly in older adults, intrinsic fibrosis or infiltration (e.g., with amyloidosis) causing “sick sinus syndrome” or due to multiple drugs. An important cause of prolonged sinus pauses is the spontaneous cessation of atrial fibrillation in patients with the paroxysmal form of this syndrome. The overdrive suppression of the sinus node during atrial fibrillation may lead to episodes of asystole long enough to causes syncope, especially in older adult subjects.
Excessive levels of (or enhanced sensitivity to) a variety of drugs, singly or in combination (e.g., beta blockers, certain calcium channel blockers, digoxin, amiodarone, dronedarone, donepezil, lithium, ivabradine), must always be excluded in patients with marked sinus bradycardia, SA pauses, or sinus arrest. Other treatable causes include acute infarction (usually inferior), hypothyroidism, hyperkalemia, anorexia nervosa, severe obstructive sleep apnea, and rarely partial seizures (termed ictal bradycardia). Prominent sinus bradycardia, and rarely sinus arrest, may occur with vasovagal (neurocardiogenic) syncope.

Chapter 13: Questions
1. Is sinus rhythm present in the following ECG?

2. Is sinus rhythm present in this ECG?

3. Which ONE of the following drugs is not a potential cause of sinus bradycardia?
a. Amiodarone
b. Ivabradine
c. Verapamil
d. Isoproterenol
e. Donepezil
f. Edrophonium
4. True or false: Respiratory sinus arrhythmia (RSA) is a physiologic finding in healthy young adults and is related to phasic changes in cardiac vagal (parasympathetic) tone modulation.

Chapter 13: Answers
1. Yes. The P waves are negative in lead aVR and positive in lead II. Do not be confused by the unusual QRS complexes (positive in lead aVR and negative in lead II) associated with the abnormal axis deviation. The diagnosis of sinus rhythm depends only on the presence of P waves and their polarity (axis).
2. No. Each QRS complex is preceded by a P wave. However, notice that the P waves are negative in lead II. These retrograde P waves indicate an ectopic pacemaker, probably located in a low atrial site near but above the AV junction.
3. d
4. True

Chapter 14: Supraventricular Arrhythmias, Part I: Premature Beats and Paroxysmal Supraventricular Tachycardias (PSVTs)

Review
Tachyarrhythmias, both supraventricular and ventricular, usually start with premature beats that initiate the sequence of rapid heartbeats by either focal or reentrant mechanisms.
Focal tachycardias involve repetitive firing of an ectopic (non-sinus) pacemaker. In contrast, reentry involves uneven (nonuniform) spread of a depolarization wave through one pathway in the heart, with blockage along a second pathway. If this block in the other pathway is “unidirectional,” the wave may be able to reenter this second pathway from the reverse direction and then travel down pathway 1, creating an abnormal “revolving door” (reentrant) circuit.
Premature supraventricular atrial (or junctional) complexes or beats (PACs or APBs, synonymously) result from ectopic stimuli: beats arising from loci in the left or right atrium, the interatrial septum, the pulmonary vein areas, or the AV junction area, but not the sinoatrial (SA) node, itself. The atria, therefore, are depolarized from an outlying or ectopic site. After an atrial (or junctional) premature depolarization, the stimulus may spread normally through the His–Purkinje system into the ventricles. For this reason, ventricular depolarization (the QRS complex) is generally not affected by PACs or junctional premature beats. However, if a PAC comes very soon after the preceding beat, the premature P wave may not conduct to the ventricles (blocked PAC). In other cases, the premature supraventricular beat may conduct through the AV junction but part of the bundle branch system may still be refractory (producing a wide QRS complex, so-called aberration or aberrancy).
PACs, conducted and blocked, are common in individuals with normal hearts and any type of heart disease. Very frequent PACs are sometimes the forerunner of atrial fibrillation or flutter or paroxysmal supraventricular tachycardias (PSVTs). There are three major classes of PSVT: (1) atrial tachycardia (AT); (2) AV nodal reentrant tachycardia (AVNRT); and (3) AV reentrant (bypass tract-mediated) tachycardia (AVRT).
Classic (unifocal) atrial tachycardia (AT) is defined as three or more consecutive PACs originating from a single atrial focus and having an identical, non-sinus P wave morphology. The arrhythmia focus can be located in either the left or right atrium or proximal pulmonary vein area. These atrial cells may fire off (depolarize) “automatically” in a rapid way, exceeding the sinus rate. An important variant, often associated with severe chronic obstructive lung disease, is multifocal atrial tachycardia (MAT), in which the P waves vary from beat to beat because they come from different “firing” sites.
AV nodal reentrant (reentry) tachycardia (AVNRT) is a form of PSVT resulting from reentry in the AV node area. Normally, the AV node behaves as a single conductor connecting the atria and His–Purkinje–ventricular electrical network. However, in some people, the AV node region has two functional conduction channels with different electrical properties (so-called dual pathways). One AV nodal pathway has fast conduction/slow recovery and the other has slow conduction/fast recovery properties. These disparities in conduction and recovery times allow for reentry to occur, especially after a premature atrial complex.
AVNRT produces a rapid and almost metronomically regular supraventricular rhythm with rates usually between 140 and 220 or so beats/min. Typically, AVNRT occurs in normal hearts and starts at a young age, most commonly in young women. Until the arrhythmia is correctly identified, many of these patients are misdiagnosed as having anxiety or panic attacks. The most common presenting symptom is palpitations. Patients may also report dyspnea or lightheadedness (rarely frank syncope). In cases where major obstructive coronary disease is present, sustained PSVTs may cause angina or dyspnea.
AVRT involves an accessory tract, which provides the substrate for reentry. Bypass tracts are designated as either manifest or concealed. Manifest bypass tracts can conduct the electrical signal in both directions: from the atria to the ventricles and in reverse. During sinus rhythm, this produces the classic triad (“signature”) of the WPW pattern: delta wave, short PR interval, and wide QRS complex (see Chapter 18).
The majority of bypass tracts, however, do not conduct the impulse from the atria to the ventricles and are, therefore, invisible (concealed) during sinus rhythm. Thus, you will not see the classic WPW signature. However, some concealed bypass tracts can conduct the impulse in the reverse (retrograde) direction (from ventricles to atria), providing, in concert with the AV node and infranodal conduction system, the second pathway necessary for reentry. This large circuit is the basis for a narrow complex tachycardia, referred to as orthodromic AVRT. The term “orthodromic” means that the impulse travels initially in the usual (“ortho” = “correct”) direction—going down the AV junction/bundle branch system (antegrade part of circuit) and then reentering the atria via the concealed bypass tract (retrograde part of circuit).
The first episode of AVRT usually occurs in childhood or young adulthood. In contrast to AVNRT, predominantly seen in young to middle-aged female subjects, AVRT occurs more frequently in men. The accessory bypass tracts can be located on the left or right side of the heart (see Chapter 18). The symptoms, including palpitations and lightheadedness, as well as shortness of breath, are similar to AVNRT, discussed previously.
The differential diagnosis of PSVT can be difficult, even for seasoned cardiologists. Sometimes it is impossible to tell the exact mechanism of the arrhythmia from the surface electrocardiogram (ECG) (especially when its initiation and termination), unless an invasive electrophysiologic (EP) study is performed.
The most clinically useful diagnostic as well as therapeutic measures in terminating reentrant PSVTs (AVNRT and AVRT) are aimed at achieving a sufficient degree of slowing in AV node conduction. These acute measures include (1) vagal maneuvers, particularly the Valsalva maneuver and carotid sinus massage (CSM) and (2) pharmacologic interventions, especially adenosine injection, as well as verapamil or diltiazem, beta blockers, or less commonly in selected cases, digoxin.
Long-term PSVT management depends on the episode frequency and degree of symptoms. If episodes are rare and mild, no specific treatment is necessary after termination. If episodes are frequent, sustained, or sufficiently symptomatic, prophylactic treatment with AV nodal blocking agents or antiarrhythmic drugs may be warranted. Timely referral to an electrophysiology specialist is justified as the efficacy of ablation procedures is very high, with attendant low risks when done by experienced operators.
PSVT, unlike atrial fibrillation or flutter, does not increase thromboembolic risk. Therefore, anticoagulation is not indicated.

Chapter 14: Questions
1. Based on the rhythm strip shown here, why might this patient complain of occasional palpitations?

2. What is the beat marked X?

3. Examine the rhythm strip shown here and answer the following questions. (Vertical marks are at 3-sec intervals.)

a. What is the approximate resting heart rate of this narrow, regular complex tachycardia from a 45-year-old woman with the sudden onset of palpitations?
b. What type of tachyarrhythmia is present?
1. Sinus tachycardia
2. Paroxysmal supraventricular tachycardia (PSVT), probably AVNRT
3. Atrial flutter
4. Atrial fibrillation
5. Multifocal atrial tachycardia
4. True or false: Paroxysmal supraventricular tachycardia (PSVT) represents sinus tachycardia at a very rapid rate at rest (above 150 beats/min).

Chapter 14: Answers
1. The palpitations (“skipped beat sensation”) could be due to occasional atrial (supraventricular) premature beats. Notice that the fifth complex is an atrial premature beat (or possibly a junctional premature beat because the P wave is not seen).
2. Junctional escape beat. Notice that this beat comes after a pause in the normal rhythm and is not preceded by a P wave.
3.
a. Approximately 210 beats/min. Count the number of QRS complexes in 6 sec and multiply by 10.
b. Paroxysmal supraventricular tachycardia (PSVT).
4. False. PSVT is not a sinus rhythm variant but is caused by mechanisms where the site or sites of stimulation are outside the sinus node. Specifically, PSVT usually involves stimulus formation in (1) one or more areas of the atria (atrial tachycardias) or a reentrant circuit in (2) the AV node area (AVNRT) or involving an atrioventricular bypass tract (AVRT).

Chapter 15: Supraventricular Arrhythmias, II: Atrial Flutter and Atrial Fibrillation

Review
Atrial fibrillation (AF) and atrial flutter are two related arrhythmias associated with very rapid atrial rates. Furthermore, both involve reentrant mechanisms. Instead of true (discrete) P waves, one sees continuous F (flutter) or f (fibrillatory) electrical activity.
The large reentrant circuit of “typical” atrial flutter (sometimes referred to as macro-reentrant atrial tachycardia) involves a circulating wave of activation that rotates in a counterclockwise direction, looping around the tricuspid valve region and up the interatrial septum. This mechanism is associated with the “sawtooth” morphology of F waves, which are predominantly negative in leads II, III, and aVF and positive in lead V1. A very regular ventricular (QRS) rate of about 150 beats/min is commonly seen due to functional 2:1 AV block (i.e., two flutter waves per each conducted QRS complex). Less frequently, the same type of circuit is initiated in the opposite direction, producing “clockwise” flutter. The polarity of the F waves will then be reversed, that is, positive in II, III, aVF, and negative in V1. Higher degrees of AV block, including complete heart block, may be seen with atrial flutter and are associated with a very slow, regularized QRS rate. Much less commonly, atrial flutter with 1:1 conduction occurs. Because of the very rapid ventricular response (around 300/min), this arrhythmia is a medical emergency. Atrial flutter with variable and frequently changing degrees of block (e.g., 2:1; 4:1, etc.) is quite common, especially after drug therapy. Clinically, the development of atrial flutter usually indicates the presence of structural/electrical atrial disease.
Unlike with atrial flutter, the focus of stimulation in AF cannot be localized to any repetitive, stable circuit in the atria. Most cases of atrial fibrillation are thought to originate in the outflow area of pulmonary vein–left atrial junctions. With time, more and more of the atrial tissue becomes involved in the active maintenance of the arrhythmia, associated with the formation of multiple, small, and unstable reentrant circuits throughout the atria. Thus, atrial electrical activity on the electrocardiogram (ECG) appears as very rapid (350-600 cycles/sec) irregular f (fibrillatory) waves, varying continuously in amplitude, polarity (reversing from positive or negative orientation in same lead), and frequency (changing cycle length, measured as the very brief interval from one f wave to the next).
Usually, the best leads to identify the diagnostic irregular atrial activity of AF are leads V1 and lead II. These leads are also often the most useful to detect atrial flutter waves.
In atrial fibrillation the AV node gets bombarded with these highly disorganized impulses of different intensity. Most of the signals are blocked in the node due to its inherent refractoriness, and only a fraction conduct to the ventricles. Still, in the absence of AV nodal disease or certain drugs (especially beta blockers, calcium channel blockers, and digoxin), the mean resting ventricular rate in AF is relatively high. Furthermore, inappropriate increases can occur during even mild exertion. Because of random penetration of the impulses through the AV node, the RR intervals in atrial fibrillation are haphazardly irregular. However, at very ventricular rapid rates, this irregularity may be difficult to detect, leading to incorrect diagnoses (“pseudo-regularization”).
Although atrial flutter almost always occurs in the setting of manifest structural heart disease, atrial fibrillation occasionally develops in apparently normal hearts. AF and flutter can also occur in the same patient, with abrupt transitions from one rhythm to the other. Although by ECG appearance these rhythms can appear quite similar, it is important to distinguish between them because of differences in management. In particular, atrial flutter has a higher rate of sustained success with radiofrequency ablation than does AF.
AF is the most common arrhythmia causing hospital admissions. Over 2 million Americans have intermittent or chronic AF, and the incidence rises with age. An estimated 10% or more of individuals 80 years or older in the United States develop AF. In some patients, AF occurs paroxysmally and may last only minutes or less, hours, or days. Some patients may experience only one episode or occasional episodes, whereas others have multiple recurrences. In some patients, AF is more persistent and may become permanent (chronic), lasting indefinitely.
During the episodes, some patients are quite symptomatic (often complaining of palpitations, fatigue, dyspnea, lightheadedness, or chest discomfort), whereas others, surprisingly, have no specific complaints. Frank syncope is uncommon but can occur, especially as the result of long post-conversion pauses upon arrhythmia self-termination, an example of the “tachy-brady syndrome.”
In the asymptomatic patient, AF may first be discovered during a routine or preoperative examination or when the patient presents with heart failure or stroke. AF can occur in people with no detectable heart disease and in patients with a wide variety of cardiac diseases. The term lone atrial fibrillation has been used to describe recurrent or chronic AF in patients without clinically apparent evidence of heart disease. Paroxysmal AF may occur spontaneously without apparent cause, or it may be associated with stress or excessive alcohol consumption in otherwise healthy individuals (holiday heart syndrome).
AF is one of the most frequently observed arrhythmias in patients with organic (structural) heart disease (resulting from hypertension, coronary disease, valvular disease, cardiomyopathy, etc.). The prevalence of this arrhythmia rises with advancing age. Numerous other conditions can also lead to AF. For example, patients with thyrotoxicosis (hyperthyroidism) may develop AF. The arrhythmia (or atrial flutter) is quite common after cardiac surgery. It may also occur with pericardial disease (especially chronic), severe parenchymal lung disease, acute or recurrent pulmonary emboli, virtually any cardiomyopathy, congenital heart disease (e.g., atrial septal defect), and other forms of heart disease. Obstructive sleep apnea (OSA) is associated with an increased risk of AF.
Changes in autonomic tone may help provoke AF in susceptible individuals. Sometimes the arrhythmia is related to increased sympathetic tone (e.g., occurring during strenuous exercise or with emotional excitement). In other cases, AF has been reported in the context of sustained high vagal tone (e.g., in elite endurance athletes).
AF and atrial flutter have two major clinical implications. First and foremost is the increased thromboembolic risk (most importantly, stroke). Therefore, whenever either is detected, the anticoagulation status of the patient should be reviewed and appropriate, personalized treatment promptly initiated. Anticoagulation should not be delayed pending rate control. Clinicians should be aware that thromboembolic risk is increased, not only in persistent or chronic AF but in patients with paroxysmal AF as well. Stroke risk is highest in patients with AF associated with valvular heart disease (especially mitral) and in those with prosthetic heart valves. Estimation of stroke risk in AF/flutter in “nonvalvular AF” depends on the presence or absence of selected comorbid conditions and demographic factors, including older age (≥65 years) and history of one or more of the following: hypertension, stroke or transient ischemic attacks, diabetes mellitus, and congestive heart failure. Female gender and vascular disease (e.g., peripheral arterial disease, including MI) are also now known to confer an increased risk of stroke.
Depending on the estimated risk, oral anticoagulation regimens may include warfarin or one of the newer (non-vitamin K antagonists) anticoagulant agents (formerly designated as NOACs) in selected patients with nonvalvular AF. These drugs are now referred to as direct oral anticoagulants (DOACs).
The second important clinical implication of AF/flutter is the risk of developing or exacerbating heart failure. This complication is due to decreased cardiac output from lack of atrial contraction in AF, especially in concert with a rapid and irregular rate.
There are two general treatment strategies for long-term management of persistent or permanent atrial fibrillation and flutter: rate control and rhythm control.
Rate control centers on limiting the ventricular response to a physiologic range, without attempts at restoring sinus rhythm. Rate control can be achieved by using AV nodal blocking agents (e.g., beta blockers, calcium channel blockers, digoxin) or AV junctional (AVJ) ablation. AVJ ablation (with pacemaker implantation) is reserved for patients whose ventricular rate cannot be effectively controlled with medications. It is a percutaneous procedure electrically “disconnecting” the atria from the ventricles and achieving excellent rate control without any further need for AV nodal blocking agents. The downside of AVJ ablation is that the patient becomes largely pacemaker-dependent. As with any of the other rate-controlling options, anticoagulation has to be continued indefinitely.
Rhythm control strategy consists of two phases: (1) sinus rhythm restoration (via DC or pharmacologic cardioversion or sometimes ablation therapy) and (2) sinus rhythm maintenance with antiarrhythmic agents. Choosing between rate and rhythm control, making decisions about medications, and assessing the indications for and timing of AF ablation (pulmonary vein isolation) all need to be personalized based on current evidence. Weight loss and treatment of OSA are important components of therapy in many patients. The challenges of understanding, preventing, and treating AF represent one of the most active areas of focused cardiology research, basic and clinical.

Chapter 15: Questions
1. Answer the following questions about the monitor lead rhythm strip shown here:

a. What is the atrial rate?
b. What is the ventricular rate?
c. What is this arrhythmia?

2. Answer the following questions about this rhythm strip. (Vertical marks are at 3-sec intervals.)

a. What is the average heart rate?
b. What is the rhythm?
3. The atrial rate with atrial flutter is (faster, slower) than the atrial rate with atrial fibrillation.
4. The atrial rate with typical atrial flutter is usually (faster, slower) than that with atrial tachycardia.
5. True or false: The ventricular rate with new onset atrial fibrillation is always greater than 100 beats/min.
6. True or false: Systemic embolization causing stroke or vascular occlusion is not a risk with atrial flutter.

Chapter 15: Answers
1.
a. ∼300 beats/min
b. ∼75 beats/min
c. Atrial flutter with 4:1 AV conduction (4:1 AV block). This degree of block usually implies intrinsic AV node disease or some AV nodal suppressant medication.
2.
a. ∼70 beats/min. Count the number of QRS complexes in 6 sec and multiply by 10.
b. Atrial fibrillation. This is a subtle example because the fibrillatory waves are of very low amplitude. The diagnosis of atrial fibrillation should always be considered when an irregular ventricular response is found along with fine wavering (fast oscillations) of the baseline between QRS complexes.
3. Slower
4. Faster
5. False
6. False

Chapter 16: Ventricular Arrhythmias

Review
Premature ventricular complexes (PVCs), also called premature ventricular beats or depolarizations, may occur without cardiac abnormalities or with any type of organic heart disease. PVCs, as implied by the name, have the following characteristics:

1. They are premature, occurring before the next beat is expected.
2. They have an aberrant shape. The QRS complex is abnormally wide, usually 0.12 sec or more in duration, and the T wave and QRS complex usually point in opposite (discordant) directions.

PVCs may occur sporadically or frequently. Two PVCs in a row are called a couplet. Three or more in a row at a rate of ≥100 min constitute ventricular tachycardia (VT). When a PVC occurs after each supraventricular (usually, but always sinus) beat, the grouping is called ventricular bigeminy. Sequences of two supraventricular beats followed by a PVC constitute ventricular trigeminy.
A PVC is often followed by a compensatory pause before the next normal sinus QRS. Uniform PVCs have the same shape in a single lead. Multiform PVCs have different shapes in the same lead.
A PVC occurring simultaneously with the apex of the T wave of the preceding beat constitutes the “R on T phenomenon.” This short coupling may be the precursor of VT or ventricular fibrillation (VF), particularly in the setting of acute myocardial ischemia/infarction or long QT syndromes.
VT is usually described clinically on the basis of duration and morphology. Short runs of VT are called nonsustained. In sustained VT, episodes usually last more than 30 sec and may lead to syncope or even cardiac arrest. VT is also classified as monomorphic or polymorphic.
Accelerated idioventricular rhythm (AIVR) is a ventricular arrhythmia (usually monomorphic) that resembles a type of slow VT, with a rate between 50 and 100 beats/min. AIVR may be seen with acute MI (especially during reperfusion), where it is typically self-limited.
Monomorphic VT may occur with or without identifiable structural heart disease. Examples of the former include VT associated with a prior myocardial infarction (MI) or with nonischemic cardiomyopathy. One of the most common examples of VT occurring without identifiable heart disease is that originating in the right ventricular outflow tract (RVOT).
Polymorphic ST is classified based on whether there is QT prolongation or not in underlying supraventricular beats. Torsades de pointes is a specific form of polymorphic VT in which the QRS complexes in the same lead appear to “twist” periodically and turn in the opposite direction. Torsades is seen in the setting of delayed ventricular repolarization (increased QT interval and/or prominent U waves) caused by drugs (e.g., quinidine, procainamide, disopyramide, dofetilide, ibutilide, sotalol), electrolyte abnormalities (hypokalemia, hypomagnesemia), or other factors summarized in Chapter 25, including high-degree AV block and inherited “channelopathies.”
Polymorphic VT also may occur with a normal or even short QT in the setting of acute ischemia or excess catecholamines (see Chapter 21).
When ventricular fibrillation (VF) occurs, the ventricles cease pumping and, instead, fibrillate or twitch in an ineffective fashion. VF (along with pulseless ventricular tachycardia) is one of the three major classes of ECG patterns seen during cardiac arrest; the other two are brady-asystole and pulseless electrical activity (see Chapter 21).

Chapter 16: Questions
1. What is the arrhythmia shown here? (Vertical marks are at 3-sec intervals.)

2. Which arrhythmia does this rhythm strip show?

3. Name three potentially treatable causes of premature ventricular complexes (PVCs).
4. What is the rhythm shown here?

5. This ECG, from a 70-year-old woman, is most consistent with which ONE of the following diagnoses?

a. Sinus tachycardia with right bundle branch block (RBBB)
b. Atrial flutter with 2:1 AV conduction along with RBBB
c. Monomorphic ventricular tachycardia
d. AV nodal reentrant tachycardia (AVNRT) with RBBB
e. Atrial tachycardia (AT) with RBBB

Chapter 16: Answers
1. Ventricular tachycardia (monomorphic)
2. Torsades de pointes type of polymorphic ventricular tachycardia (VT). Notice the systematically changing orientation and amplitude of the QRS complexes in any given lead (but necessarily all leads) with this type of VT. The QT interval of the single supraventricular beat at the end is prolonged. Contrast this with the monomorphic VT in question 1, in which all QRS complexes have the same morphology in any given lead.
3. Hypoxemia, digoxin excess or certain other drug toxicities, hypokalemia, and hypomagnesemia, among others (see text)
4. Sinus bradycardia with ventricular bigeminy
5. c. Monomorphic ventricular tachycardia (VT). The ECG shows a very regular, wide (broad) complex tachycardia (about 200 beats/min) with an RBBB morphology. No atrial (flutter or true P) waves are evident. (The notches in the QRS are not P waves but part of the QRS itself.) Strongly in favor of VT are (1) the very wide QRS complexes (about 160 msec, measured in lead V3); (2) the Rsr′ (initial R taller than second one; or broad R wave or qR wave) in lead V1; and (3) the initial wide Q wave in lead I. (QS waves are also noted in the inferior and lateral leads.) The patient had sustained a prior inferior-posterior-lateral ST elevation/Q wave MI and underwent implantable cardioverter–defibrillator (ICD) placement for sustained ventricular tachycardia originating in the area of the extensive ventricular scar. See Chapter 19.

Chapter 17: Atrioventricular (AV) Conduction Abnormalities: Part I: Delays, Blocks, and Dissociation Syndromes

Review
Clinicians should address three major issues related to apparent abnormalities in AV conduction: (1) What is the degree of AV block: first, second, or third degree? (2) What is the likely level of the AV block: nodal or infranodal? (3) What is the likely cause of the AV block? The answers will help determine what, if any, further evaluation or therapy is required and especially whether a temporary or permanent pacemaker (Chapter 22) is indicated.
First-degree AV block is characterized by a P wave (usually sinus in origin) followed by a QRS complex with a prolonged PR interval >200 msec. The PR may be uniformly prolonged or may vary from beat to beat. Some clinicians prefer the more descriptive term PR interval prolongation because the signal is not really blocked; rather it is delayed.
Second-degree AV block is characterized by intermittently blocked (or “dropped”) QRS complexes. There are two major subtypes of second-degree AV block: Mobitz type I (Wenckebach) and Mobitz type II.

1. With sinus rhythm with Mobitz type I, which is the classic AV Wenckebach pattern, each stimulus from the atria has progressive “difficulty” traversing the AV node to the ventricles (i.e., the node becomes increasingly refractory). Finally, the cycle ends when an atrial stimulus is not conducted at all and the expected QRS complex is blocked (the “dropped QRS”). This cycle is followed by relative recovery of the AV junction; the cycle then starts again. The characteristic ECG signature of sinus rhythm with AV Wenckebach block, therefore, is of progressive lengthening of the PR interval from beat to beat until a QRS complex is not conducted. The PR interval after the nonconducted P wave (the first PR interval of the new cycle) is always shorter than the PR interval of the beat just before the nonconducted P wave.
2. Sinus rhythm with Mobitz type II AV block is a rarer and more serious form of second-degree heart block. Its characteristic feature is the sudden appearance of a single, nonconducted sinus P wave without (1) the progressive prolongation of PR intervals seen in classic Mobitz type I (Wenckebach) AV block and (2) without substantial (e.g., ≤40 msec) shortening of the PR interval in the beat after the nonconducted P wave as seen with type I block. A subset of second-degree heart block occurs when there are multiple consecutive nonconducted P waves present (P–QRS ratios of 3:1, 4:1, etc.). This finding is referred to as high-degree (or advanced) AV block. It can occur at any level of the conduction system. A common mistake is to call this pattern Mobitz type II block.

First- and second-degree heart blocks are examples of incomplete blocks because the AV junction conducts some stimuli to the ventricles. With complete (third-degree) AV heart block, no stimuli are transmitted from the atria to the ventricles. Instead, the atria and ventricles are paced independently. The atria may continue to be paced by the sinoatrial (SA) node. The ventricles, however, are paced by a nodal or infranodal escape pacemaker located somewhere below the point of AV block. The resting ventricular rate with complete heart block may as slow as 30 beats/min or less or as high as 50 to 60 beats/min. Bradyarrhythmia with CHB may be associated with QT prolongation leading to increased risk of torsades de pointes (Chapter 16).
Complete heart block may also occur in patients whose basic atrial rhythm is flutter or fibrillation. In these cases, the ventricular rate is very slow and almost completely regular.
Interruption of electrical conduction can occur at any level starting from the AV node itself (nodal block) down to the His bundle and its branches (infranodal block).
In general, block at the level of the AV node (1) is often caused by reversible factors, (2) progresses more slowly, if at all, and (3) in the case of complete heart block is associated with a relatively stable escape rhythm. In contrast, infranodal block (1) is usually irreversible and (2) may progress rapidly and unexpectedly to complete heart block with a slow, unstable escape mechanism. Therefore, infranodal block (even second-degree) generally requires pacemaker implantation.
Sinus rhythm with 2:1 AV block is usually considered as a “special” category of second-degree block and may be caused by nodal or infranodal conduction abnormalities.
Be aware that cardiologists use the term AV dissociation in two related, though not identical, ways, which may cause confusion: (1) As a general term, it is used to describe any arrhythmia in which the atria and ventricles are controlled by independent pacemakers. This definition includes complete heart block (usually requiring an electronic pacemaker) as well as some instances of ventricular tachycardia or accelerated idioventricular rhythm in which the atria remain in sinus rhythm (see Chapter 16). (2) As a more specific term, it is used to describe a particular family of arrhythmias in which the sinoatrial (SA) node and AV junction appear to be “out of sync;” thus, the SA node loses its normal control of the ventricular rate. As a result the atria and ventricles are paced independently—the atria from the SA node, the ventricles from the AV junction. This situation is similar to that which occurs with complete heart block. However, in this instance, the ventricular rate is the same as or slightly faster than the atrial rate. When the atrial and ventricular rates are almost the same, the term isorhythmic AV dissociation is used and a pacemaker is not indicated.
Clinicians should recognize the difference between AV dissociation resulting from “desynchronization” of the SA node and AV junction and actual complete heart block, which results from true AV conduction failure. With AV dissociation (e.g., isorhythmic) a properly timed P wave can be conducted through the AV junction; in contrast, with complete (third-degree) heart block, no P wave can stimulate the ventricles because of severed electrical signaling between the upper and lower cardiac chambers.

Chapter 17: Questions
. This rhythm strip shows sinus rhythm in concert with which ONE of the following?

a. Wenckebach-type (Mobitz type I) second-degree AV block
b. Complete (third-degree) AV heart block
c. 3:1 AV heart block
d. Isorhythmic AV dissociation
e. Blocked premature atrial complexes (PACs)

2. Based on this rhythm strip, answer the following questions:

a. What is the approximate atrial (P wave) rate?
b. What is the approximate ventricular (QRS) rate?
c. Is the PR interval constant?
d. What ECG abnormality is shown?

3. What two major findings does this lead II rhythm strip show from an older adult man with dizziness and weakness?

4. What is the rhythm in this ECG? (Note the baseline artifact in V4.)

5. What is the mechanism of the pauses in the following ECG, obtained from an older adult patient with episodic lightheadedness? Note the QRS complexes show a right bundle branch block (RBBB) with an indeterminate axis. The inferior Q waves are nondiagnostic but raise consideration of prior inferior MI. Nonspecific ST-T abnormalities are present in multiple leads.

a. Sinus rhythm with Mobitz I (nodal) AV block (Wenckebach)
b. Sinus rhythm with Mobitz II (infranodal) AV block
c. Sinus with blocked premature atrial complexes (PACs)
d. Accelerated idioventricular rhythm (AIVR)
e. Sinus rhythm with complete (third-degree) AV block

Chapter 17: Answers
1.
a. Sinus rhythm with AV Wenckebach block. Notice the regular succession of P waves, with increasing PR intervals followed by a “dropped” (nonconducted) P wave. This mechanism (as well as Mobitz II AV block) leads to “group beating.” Blocked premature atrial complexes can also cause a similar group beating pattern, but the nonconducted P waves will come early (before the next sinus P wave is due). The P waves in this example come “on time,” that is, they are not premature, allowing one to distinguish second-degree AV block (Mobitz 1 or 2) from blocked APBs as causes of the group beating “phenotype.”
2.
a. ∼100 beats/min
b. ∼42 beats/min
c. No
d. Sinus rhythm with complete AV heart block. Notice that some of the P waves are “hidden” in QRS complexes or T waves.
3. Atrial fibrillation with complete heart block (CHB). Note the fibrillatory activity of the baseline (see magnified image) between the regular and slow QRS complexes at a rate of <45 beats/min. This patient required a permanent pacemaker as well as anticoagulation for the atrial fibrillation. In cases of CHB, you must always specify the atrial mechanism (e.g., sinus, atrial fibrillation, atrial flutter, etc.). Stating that the rhythm is “complete heart block” is not a complete reading. The added level of detail about the atrial mechanism is crucial because patients with underlying sinus rhythm and CHB benefit from a dual-chamber pacemaker, while those with permanent atrial fibrillation would get only a ventricular pacemaker because atrial pacing (“capture”) is not possible. Furthermore, they would be candidates for anticoagulation because of thromboembolic risk. See Chapter 22.
4. Sinus bradycardia at a rate ∼40 beats/min with isorhythmic AV dissociation (junctional rhythm at about the same rate). Note how the sinus P waves appear to “slide” in and out of the normal (narrow) QRS complexes. This rhythm is attributable to the combination of a slow sinus rate with a junctional escape mechanism that behaves as though both rhythms are “competing” with each other but slightly “out of sync.” Of key importance is the fact that this type of AV dissociation is not a form of complete heart block. Instead, this type of AV “desynchronization” is usually a benign, transient, and reversible occurrence. Possible causes include increased physiologic increases in vagal tone (e.g., during sleep) or drugs (e.g., beta blockers, calcium channel blockers).
5. b. Note that sinus rate is about 75/min, the PR intervals of the conducted beats are within normal limits and the same before conducted and after the nonconducted “dropped” P waves, which come abruptly. The bundle branch disease in concert with this Mobitz II pattern of second-degree AV block point to an infranodal conduction impairment and the need for a pacemaker. The fact that the nonconducted P waves come “on time” (and are not early) rules out premature atrial complexes. With AV Wenckebach, the PR after a nonconducted P wave is substantially shorter than the one before the nonconducted P wave.

Chapter 18: Atrioventricular (AV) Conduction Abnormalities, Part II: Preexcitation (Wolff–Parkinson–White) Patterns and Syndromes

Review
The Wolff–Parkinson–White (WPW) pattern results from preexcitation of the ventricles via a manifest bypass tract (accessory pathway) connecting the atria and ventricles, thereby short-circuiting the AV node. As a result, during sinus rhythm the electrocardiogram (ECG) classically shows a triad of findings consisting of (1) a short PR interval; (2) a wide QRS complex; and (3) slurring or notching of the initial part of the QRS, referred to as a delta wave. Some patients with WPW have multiple bypass tracts.
Patients with the WPW pattern are particularly prone to attacks of a specific reentrant-type paroxysmal supraventricular tachycardia (PSVT), which may cause palpitations, shortness of breath, or even syncope. The group of reentrant tachycardias that utilize a bypass tract is formally termed atrioventricular reentrant tachycardia (AVRT). Sometimes the older term AV reciprocating tachycardia is used.
If the tachycardia conduction circuit involves the wavefront going down the AV node/His–Purkinje system and then back up to the atria via the bypass tract, the term orthodromic AVRT applies. In such cases, a narrow complex tachycardia (NCT) will be seen (unless a bundle branch block is present). If the tachycardia involves conduction down the bypass tract and back up the AV junction into the atria, a wide complex tachycardia (WCT) will be seen (antidromic type of AVRT).
Clinicians should also be aware that an important subgroup of patients with narrow complex tachycardias due to AVRT have an accessory pathway that is concealed. In these patients, the bypass tract cannot conduct downward (antegrade) from atrial to ventricles but may only conduct in a retrograde direction, thereby supporting a reentrant tachycardia. This mechanism is discussed in Chapter 14.
Less commonly, WPW may be associated with atrial fibrillation (AF), causing a very fast ventricular rate with a WCT. If the rate becomes extremely rapid, this rhythm may lead to (degenerate into) ventricular fibrillation with sudden cardiac arrest.
The term WPW syndrome applies to patients who have PSVT or atrial fibrillation related to one or more bypass tract(s). Symptomatic WPW syndrome is curable in most cases by catheter ablation of the accessory pathway during a cardiac electrophysiology (EP) procedure.

Chapter 18: Questions
1. The wide QRS here is attributable to which ONE of the following?

a. Right bundle branch block
b. Tricyclic antidepressant (TCA) toxicity
c. Posterolateral myocardial infarction (MI)
d. Wolff–Parkinson–White (WPW) preexcitation pattern
e. Hyperkalemia

2. The wide QRS in the following ECG is attributable to which ONE of the following mechanisms?

a. Sinus tachycardia with left bundle branch block
b. Sinus tachycardia with left ventricular hypertrophy
c. Sinus tachycardia with Wolff–Parkinson–White pattern
d. Sinus tachycardia with left anterior fascicular block
e. Ventricular tachycardia (monomorphic)

Chapter 18: Answers
1. d. The ECG shows sinus rhythm with a WPW pattern. Notice the diagnostic WPW triad: (1) wide QRS complex, (2) short PR interval, and (3) delta wave (slurred or notched initial portion of the QRS complex). WPW patterns are sometimes mistaken for hypertrophy (tall R waves) or MI (pseudo-infarction Q waves). The delta wave is typically negative in leads reflecting the earliest part of the ventricles to be depolarized. The negative delta wave in lead aVL and positive delta wave in lead V1 are consistent with a left lateral wall bypass tract in this case.
2. c. This ECG also shows the classic WPW triad. The polarity of the delta wave (negative in V1 and positive laterally) is consistent with a right-sided bypass tract. The anomalous conduction pattern in WPW in this case might be mistaken for left ventricular hypertrophy, left bundle branch block, or prior inferior Q wave infarction.

Part III: Special Topics and Reviews

Chapter 19: Bradycardias and Tachycardias: Review and Differential Diagnosis

Review
Arrhythmias can be conveniently grouped into bradycardias (resting heart rate slower than 50-60 beats/min) and tachycardias (resting heart rate faster than 100 beats/min).
Bradycardias include five major classes of arrhythmias or conduction disturbances:

1. Sinus bradycardia and related variants, such as wandering atrial pacemaker and slow ectopic atrial escape rhythms
2. Atrioventricular (AV) junctional (nodal) escape rhythms
3. Second- or third-degree AV heart block (or some forms of AV dissociation)
4. Atrial fibrillation or flutter with a slow ventricular rate
5. Idioventricular escape rhythm (IVR), excluding severe hyperkalemia

These categories are not mutually exclusive. For example, third-degree AV block is usually accompanied by a junctional or idioventricular escape rhythm (preventing asystole and cardiac arrest).
Bradycardias should prompt a search for reversible causes (drugs, hyperkalemia, ischemia, etc.) or may be caused by degenerative changes in the conduction system leading to sick sinus syndrome or nodal or infranodal conduction disease.
Tachycardias can be most usefully classified into (1) those with narrow (normal duration) QRS complexes (narrow complex tachycardias [NCTs]) and (2) those with wide (broad) QRS complexes (wide complex tachycardias [WCTs]).
Narrow-complex QRS tachycardias are almost always supraventricular in origin and include the following:

1. Sinus tachycardia (appropriate and inappropriate)
2. Paroxysmal (or persistent) supraventricular tachycardias (PSVTs), including atrial tachycardia (AT), AV nodal reentrant tachycardia (AVNRT), and AV reentrant tachycardia (AVRT)
3. Atrial fibrillation (AF)
4. Atrial flutter

NCTs can be either regular or irregular. NCTs with a metronomically regular QRS rate (cadence) include sinus tachycardia (especially at very fast rates), atrial flutter with 2:1 (or rarely 1:1) conduction, and most PSVTs. NCTs with an irregular rate include sinus tachycardia with frequent, unifocal premature atrial beats, atrial fibrillation, atrial flutter with variable block, and multifocal atrial tachycardia (MAT).
Vagal maneuvers, including the Valsalva maneuver and carotid sinus massage, are sometimes helpful in differentiating these arrhythmias at the bedside.
Tachycardias with wide QRS complexes (WCTs) may represent either ventricular tachycardia (VT) or any of the supraventricular tachycardias listed previously, in association with (1) a bundle branch block (or equivalent type of aberrancy) or (2) with anomalous conduction due to a Wolff–Parkinson–White preexcitation mechanism. Discriminating VT from SVT with aberration/anomalous conduction is a frequent problem encountered in the emergency department and critical care units. Before applying any ECG-based diagnostic algorithms to WCT differential diagnosis, clinicians should take into account the fact that over 80% of WCTs presenting to medical attention in adults are VTs. In patients with known structural heart disease (e.g., prior infarcts, cardiomyopathies) this percentage increases to over 90%.
A variety of ECG parameters may be useful in differentiating VT from SVT with aberrancy from the 12-lead ECG. However, no set of criteria or current algorithm has 100% sensitivity and 100% specificity. The presence of AV dissociation is virtually diagnostic of ventricular tachycardia. The morphology of the QRS in leads V1/V2 and V6, the presence of positive or negative QRS concordance, QRS duration, and comparison with previous ECGs may all be helpful, as discussed in the text.
The term sick sinus syndrome applies to patients with sinoatrial (SA) node dysfunction who have an inappropriate, marked sinus bradycardia (sometimes with sinus arrest or slow junctional escape rhythms), which may cause lightheadedness or frank syncope. Some patients with sick sinus syndrome have periods of tachycardia alternating with the bradycardia (tachy-brady or brady-tachy syndrome).

Chapter 19: Questions
1. Answer the following questions about this lead II rhythm strip:

a. Is the rate regular or irregular?
b. Are discrete P waves present?
c. What is this arrhythmia?

2. What is the most likely diagnosis for the arrhythmia shown in this monitor lead?

3. What is the cause of the bradycardia in this rhythm strip?

4. Identify at least five reversible pharmacologic or metabolic causes of bradycardia.
5. What is this bradyarrhythmia that was recorded during sleeping hours? Is a pacemaker indicated? Note: This recording is from a Holter ECG, using modified leads II and V1. Vertical marks are at 3-sec intervals.

6. This Holter monitor rhythm strip (modified lead II) was recorded during waking hours from an older adultwoman with lightheadedness. What rhythm does it show? Vertical marks at 3-sec intervals.

7. This wide complex tachycardia (WCT) is most consistent with which ONE of the following diagnoses?

a. Atrial fibrillation with WPW conduction
b. Atrial flutter with WPW conduction
c. Polymorphic ventricular tachycardia (VT)
d. Monomorphic ventricular tachycardia (VT)
e. Multifocal atrial tachycardia (MAT) with right bundle branch block

Chapter 19: Answers
1.
a. This is an irregular, narrow complex tachycardia.
b. No. The baseline shows an irregular fibrillatory pattern but no discrete P waves.
c. Atrial fibrillation
2. Ventricular tachycardia
3. Sinus rhythm with 2:1 AV block, indicated by a sinus rate of about 74 beats/min and a ventricular rate (narrow QRS) of about 37 beats/min, with a constant PR interval in conducted beats.
4. Excess beta blocker, excess calcium channel blocker (especially, verapamil or diltiazem), amiodarone, dronedarone, lithium carbonate, donepezil, hyperkalemia, hypothyroidism, ivabradine, digoxin toxicity, among multiple others
5. The rhythm is sinus bradycardia (at about 44/min) with a wandering atrial pacemaker (WAP) variant. Note the subtle modulation in P wave orientation, attributable to a shift in the atrial pacing site from the sinus node to other supraventricular loci. Sinus bradycardia with WAP may be seen as a normal variant during sleeping hours, attributable to physiologic increases in cardiac vagal tone modulation. There is no indication for consideration of an electronic pacemaker here. Very prominent sinus pauses, and even sinus arrest, are occasionally observed with severe obstructive sleep apnea.
6. Marked sinus bradycardia with a prolonged PR interval (first-degree AV block) and a very prominent sinus pause/sinus arrest lasting almost 3 sec. The patient underwent dual-chamber pacemaker implantation for symptomatic sick sinus syndrome. As noted previously, patients with bradycardias should always be evaluated for possible reversible causes or factors (drugs, hyperkalemia, hypothyroidism, and obstructive sleep apnea, etc.) capable of exacerbating SA and AV node dysfunction. Alleviating or modifying these factors may preclude the need for an electronic pacemaker.
7. d. The ECG shows a wide complex tachycardia (WCT) diagnostic of monomorphic VT. Note the RBBB morphology with very wide QRS interval (about 240 msec in V1). Also note the QR morphology in V1 to V3 consistent with underlying anterior myocardial infarction. ST elevations in these leads raise the question of an underlying anterior aneurysm or acute ischemia. The rS complexes in V4 to V6 and the extreme right axis are also consistent with VT. The patient had severe coronary disease, with multiple prior interventional revascularization procedures, an estimated left ventricular ejection fraction of 20% and ICD placement, as well as prior ablation procedures for VT.

Chapter 20: Digitalis Toxicity

Review
Digitalis (digoxin) toxicity can produce almost any arrhythmia and all degrees of AV heart block.
However, atrial fibrillation or atrial flutter with a rapid ventricular response rarely occurs as a direct result of digitalis toxicity. Furthermore, digitalis toxicity does not produce bundle branch blocks.
Factors such as renal failure, hypokalemia, hypercalcemia, hypomagnesemia, hypoxemia, old age, and acute myocardial infarction are predisposing factors for digitalis toxicity. The concomitant administration of certain drugs (e.g., quinidine, verapamil, amiodarone, propafenone) also increases serum digoxin concentrations.
Do not confuse digitalis toxicity with digitalis effect. Digitalis effect refers to the shortening of the QT interval and associated scooping of the ST-T complex (“thumbprint sign”) produced by therapeutic doses of digitalis.

Chapter 20: Questions
1. Name three factors that can potentiate digitalis (digoxin) toxicity.

True or false (Questions 2 to 7):

2. Premature ventricular complexes (PVCs) are an important manifestation of digitalis toxicity, but most PVCs are not caused by digitalis excess.
3. Atrial fibrillation with a narrow QRS and a rapid, irregular ventricular response is a common manifestation of digitalis toxicity.
4. Left bundle branch block is a common manifestation of digitalis toxicity.
5. Sinus rhythm with Mobitz type I (Wenckebach) AV block may be caused by digitalis toxicity.
6. A serum digoxin concentration (drawn at least 6 hours after the last dose) and reported to be within the laboratory’s “therapeutic” range effectively rules out digitalis toxicity.
7. DC cardioversion is potentially very hazardous in the presence of digitalis toxicity and may lead to ventricular fibrillation.
8. The following electrocardiogram (ECG) is from an older adult woman prescribed digoxin, in addition to other medications, for heart failure with reduced left ventricular ejection fraction. It shows which ONE of the following rhythms? There is an underlying right bundle branch block (RBBB). Clue: look carefully at lead V1 for a key to diagnosing this arrhythmia.
a. Resting sinus tachycardia
b. Atrial tachycardia with 1:1 AV conduction
c. Atrial tachycardia with 2:1 AV conduction (block)
d. Atrial fibrillation with a regularized ventricular response
e. Atrial flutter with 3:1 conduction (block)

Chapter 20: Answers
1. Hypokalemia, hypomagnesemia, hypercalcemia, hypoxemia, acute myocardial infarction, cardiac amyloidosis, etc. (For other answers, please see Chapter 20.)
2. True
3. False
4. False
5. True
6. False
7. True
8. c. The rhythm is atrial tachycardia with 2:1 AV block (conduction). This rhythm occurred in the context of marked digoxin excess (serum concentration was >3.0 ng/mL). If you look carefully, especially in lead V1, you will see regularly occurring (non-sinus) P waves at a rate of about 200/min, with the regular QRS rate exactly half that (about 100/min). The ECG also shows relatively low limb voltages, prominent precordial voltages, and relatively slow R wave progression (R < S amplitude in V4). This “ECG-CHF” triad has been reported as a modestly specific but not sensitive sign of dilated cardiomyopathy (see Chapter 12). Nonspecific ST-T changes are present, consistent with digoxin effect, left ventricular hypertrophy, etc. A nondiagnostic Q wave is present in lead III.

Chapter 21: Sudden Cardiac Arrest and Sudden Cardiac Death

Review
Cardiac arrest occurs when the heart stops contracting effectively and ceases to pump blood. The diagnosis should be made clinically even before the patient is connected to an electrocardiograph. Unresponsiveness in an individual with agonal (gasping or very intermittent) or absent respiration and lack of a central (e.g., carotid or femoral) palpable pulse are the major diagnostic signs of cardiac arrest.
Cardiac arrest may be associated with one or more of the following electrocardiogram (ECG) patterns:

1. Ventricular tachyarrhythmias, including ventricular fibrillation, pulseless monomorphic ventricular tachycardia, torsades de pointes, or ventricular flutter (very rapid ventricular tachycardia with a sine-wave like appearance).
2. Ventricular standstill (asystole) or a brady-asystolic pattern, also referred to as a “flat-line” or “straight-line pattern,” sometimes associated with junctional or ventricular escape beats.
3. Pulseless electrical activity (PEA)/electromechanical dissociation (EMD), in which recurring QRS complexes and sometimes even associated P waves occur in the absence of a palpable pulse or measurable blood pressure. PEA is usually caused by diffuse myocardial injury, although it may be due to pericardial tamponade, tension pneumothorax, or massive pulmonary embolism, among other causes.

Any or all of these three patterns may be seen during the resuscitation of a patient in cardiac arrest syndrome.
With cardiac arrest the ECG also may show distinctive artifacts caused by external cardiac compression. These large, wide deflections should not be mistaken for the intrinsic electrical activity of the heart.
The term sudden cardiac arrest/death is used in reference to individuals who sustain an unexpected cardiac arrest and, unless resuscitated, die instantly or within an hour or so of the development of acute symptoms, such as chest discomfort, shortness of breath, or lightheadedness (pre-syncope or frank syncope). Sudden cardiac arrest is not a disease per se but a syndrome having multiple causes. Sudden cardiac arrest/death is also not synonymous with acute myocardial infarction (MI; “heart attack”). The latter, however, is responsible for an important subset of cases of sudden death, especially in middle-aged to older adults.
Most individuals with unexpected cardiac arrest do have underlying structural heart disease. Patients with acute MI may die suddenly before reaching the hospital, usually with ventricular fibrillation. Another important substrate for sudden death, especially in middle-aged to older adults in the United States, is ventricular tachyarrhythmia due to severe left ventricular scarring from previous MI(s).
Other patients with sudden cardiac death have structural heart disease associated with valvular abnormalities or myocardial disease: for example, severe aortic stenosis, dilated or hypertrophic cardiomyopathy, myocarditis, arrhythmogenic right ventricular cardiomyopathy (ARVC), or anomalous origin of a coronary artery.
Some individuals with sudden cardiac arrest/death do not have identifiable mechanical cardiac dysfunction but instead have the substrate for inherited or acquired electrical instability. Examples include long QT syndromes predisposing to torsades de pointes, polymorphic ventricular tachycardia with a normal QT, the short QT syndrome, the Wolff–Parkinson–White (WPW) preexcitation syndrome (e.g., associated with atrial fibrillation precipitating ventricular fibrillation), the Brugada syndrome, and severe sinoatrial (SA) or atrioventricular (AV) conduction system disease causing prolonged sinus arrest or high-grade heart block, respectively.
The Brugada syndrome refers specifically to the association of a characteristic ECG pattern with a documented occurrence or high risk (e.g., familial history of sustained ventricular tachyarrhythmias). The Brugada pattern itself consists of distinct J point/ST segment elevations in one or more of chest leads V1 to V2/V3 with a QRS pattern resembling a right bundle branch block. A rare cause of recurrent syncope and sometimes sudden cardiac death is catecholaminergic polymorphic ventricular tachycardia (CPVT), typically induced by exercise or stress. Some cases are familial (autosomal dominant), related to a genetic mutation that alters calcium dynamics in myocytes.
Multiple pharmacologic agents, such as cocaine for “recreational” use, or cardiac antiarrhythmic agents, such as flecainide, dofetilide, and quinidine, may induce lethal arrhythmias.
The term commotio cordis refers to the syndrome of sudden cardiac arrest in healthy individuals who sustain nonpenetrating chest trauma (e.g., during certain sports) triggering ventricular fibrillation. Finally, a small subset of individuals sustains cardiac arrest without having any demonstrable structural or currently identifiable electrophysiologic abnormality (idiopathic ventricular fibrillation).
The important role of implantable cardioverter–defibrillator (ICD) devices in preventing sudden death in carefully selected, high-risk patients is discussed in Chapter 22.

Chapter 21: Questions
1. Would an electronic ventricular pacemaker be of any value in treating a patient with cardiac arrest and electromechanical dissociation (EMD)?
2. Name four pharmacologic agents that can induce or contribute to cardiac arrest associated with a sustained ventricular tachyarrhythmia (i.e., ventricular fibrillation, monomorphic ventricular tachycardia, torsades de pointes, or other forms of polymorphic VT).

Chapter 21: Answers
1. No. By definition, patients with electromechanical dissociation (pulseless electrical activity) have relatively normal cardiac impulse formation and conduction. The immediate life-threatening problem is that this electrical activity is not associated with adequate mechanical (pumping) action, caued by for example diffuse myocardial injury, pericardial tamponade, or severe loss of intravascular volume. A pacemaker will be of no help in this context because the patient’s heart already has appropriate electrical stimulation.
2. Digitalis (digoxin), epinephrine, cocaine, flecainide, as well as quinidine, procainamide, disopyramide, ibutilide, dofetilide and most other “antiarrhythmic” agents.

Chapter 22: Pacemakers and Implantable Cardioverter–Defibrillators: Essentials for Clinicians

Review
This chapter gives an overview of the two major classes of therapeutic cardiac implantable electronic devices (CIEDs), namely pacemakers and cardioverter–defibrillators (ICDs). Insertable (implantable) cardiac event recorders are discussed briefly in Chapter 4.
Pacemakers are electronic devices designed to correct or compensate for abnormalities of cardiac impulse formation (e.g., sinus node dysfunction) or conduction (e.g., high-degree AV heart block). A pacemaker consists of two primary components: (1) the generator (battery and microcomputer) and (2) one or more electrodes (also called leads).
Pacemakers can be temporary or permanent. Temporary pacing is used when the electrical abnormality is expected to resolve with time. Permanent pacemakers have both the generator and electrode(s) called leads implanted inside the body. They are used for bradycardias in advanced sinus node and AV conduction disorders and to compensate for left bundle branch block conduction abnormalities by providing interventricular synchronization. This use is called cardiac resynchronization therapy (CRT) and may be accomplished by biventricular (BiV) pacing. The contemporary and rapidly evolving use of His bundle pacing and left bundle branch area pacing are briefly discussed.
All modern pacemakers are capable of sensing intrinsic electrical activity of the heart and are externally programmable (adjustable) using special computer devices provided by the manufacturers. Pacemakers are usually set to operate in an on-demand mode, providing pacing support only when the patient’s own electrical system fails.
Single-lead (or single-chamber) pacemakers are used to stimulate only one chamber (right atrium or right ventricle). In dual-chamber pacemakers, electrodes are inserted into both the right atrium and right ventricle. The circuitry is designed to allow for a physiologic interval between atrial and ventricular stimulation. This atrioventricular delay (time between atrial and ventricular pacemaker spikes) is analogous to the PR interval seen under physiologic conditions.
Historically, pacemaker programming has been described by a standard three- or four-letter code, usually followed by a number indicating the lower rate limit.

Ventricular pacing produces electrical changes in the heart that last a long time after the pacing is stopped. This process has been called cardiac memory. In patients who are paced intermittently, these changes can be seen in nonpaced beats as T wave inversions in the leads that showed predominantly negative QRS complexes during ventricular pacing (usually precordial and inferior leads). These changes look very much like T wave inversions due to myocardial ischemia (Wellens’ pattern) but can sometimes be distinguished from it by the finding of positive T waves in leads I and aVL (see Online Section 2: Supplemental Extras).
ICDs are designed to terminate life-threatening ventricular arrhythmias (VT and VF) by delivering internal direct current shock. VT can often be terminated by rapid pacing above the rate of the ventricles (anti-tachycardia pacing). All current ICDs are capable of pacing and can be single-chamber, dual-chamber, or biventricular.
Pacemakers are very reliable devices and pacemaker malfunctions are rare, especially after the acute post-implant phase. The commonly encountered problems are failure to sense, failure to pace, and failure to capture.
ICDs are much more complex devices and their malfunctions occur more often than in pacemakers. In addition to the pacing malfunctions just described, the most important tachyarrhythmia malfunctions include inappropriate therapies for SVT or over-sensing of extracardiac electrical activity (e.g., from fractured leads, electromagnetic interference).

Chapter 22: Questions
1. Which of the following is the major indication for a permanent pacemaker?
a. History of multiple prior myocardial infarctions
b. Symptomatic bradyarrhythmias
c. Digitalis toxicity
d. Ventricular bigeminy
e. Paroxysmal supraventricular tachycardia (PSVT)
2. What is shown in the following rhythm strip obtained from a patient with a ventricular pacemaker and underlying atrial fibrillation and a single premature ventricular beat (complex).
a. Failure to sense
b. Failure to pace
c. Normal pacemaker function with a ventricular premature beat
d. Failure to sense and pace

3. What chamber is being paced in the following rhythm strip?

4. Biventricular pacing (BiV), also called cardiac resynchronization therapy, is used primarily in which of the following settings?

a. Recurrent ventricular tachycardia despite medical therapy
b. Chronic heart failure (reduced systolic ejection fraction) with left bundle branch block
c. Long QT syndromes due to inherited “channelopathies”
d. Acute myocardial infarction with cardiogenic shock

5. True or false: Implantable cardioverter–defibrillators are most often employed prophylactically in the first few days of acute ST elevation myocardial infarction (STEMI).
6. True or false: Magnet application over an ICD device disables arrhythmia detection. This response is useful in a patient receiving multiple inappropriate shocks for atrial fibrillation with a rapid ventricular response or because of electrical “noise” from ICD lead fracture, both of which may be mistaken by the device for a ventricular tachycardia.
7. The computer (electronic) reading on the following electrocardiogram (ECG) was “Pacemaker rhythm. No further analysis possible.” Do you fully agree with this reading?

Chapter 22: Answers
1. b. Symptomatic bradyarrhythmias especially acquired severe high-degree AV heart block or severe sinus node dysfunction without reversible cause. Ventricular pacemakers are also used to enhance synchrony between the left and right ventricles in carefully selected patients with heart failure, especially those with reduced left ventricular ejection fraction combined with left bundle branch block.
2. b. Failure to pace. In this example of intermittent failure to pace, the fourth pacemaker spike is not followed by a QRS complex. Two of the common causes of failure to pace evidenced by a pacemaker stimulus that does not capture the ventricles are dislodgment of the electrode wire and fibrosis around the pacing wire tip. In some cases of pacemaker failure, no pacing spikes are seen because the battery has been fully utilized.
3. Atrial pacing (large pacemaker spike followed by a P wave) is present with an intrinsic (nonpaced) QRS complex that has an intraventricular conduction delay (IVCD) with a prolonged duration (interval) of about 120 msec (0.12 sec). The QT interval (0.40 sec) is also prolonged for the rate of 83 beats/min. This yields a QTc of 470 msec (0.47 sec).
4. b.
5. False
6. True
7. No! The reading should specify: “Underlying atrial fibrillation with ventricular pacing at a rate of 80/min.” Atrial fibrillation is frequently overlooked in the presence of ventricular pacing from the regularized ventricular rate when the rhythm is fully paced.

Chapter 23: Interpreting ECGs: Integrative Approach

Review
ECG “reading” requires a disciplined approach to avoid making common errors of omission and to maximize the amount of useful information you can extract from the recording. More experienced readers usually approach an ECG in several “takes,” much like their expert colleagues examine medical imaging studies. First, they get an overall gestalt, a “big picture” overview to survey the “lay of the land.” Next, they home in on each of the following 14 features, looking at single leads, usually beginning with the rhythm strip and then at various sets of leads. This process should be iterated before formulating an overall summary and integrative interpretation.

14 Features to Analyze on Every ECG

After you have carefully analyzed these 14 ECG features, you should formulate an overall interpretation based on these details and the integration of these findings in the specific clinical context. The final ECG report usually consists of the following five elements:

• Rate(s)/PR-QRS-QT/QTc intervals/QRS axis (Note: electronic analyses usually also include the mean P and T wave axes)
• Rhythm/AV conduction (latter if abnormal)
• Key waveform findings
• Clinical inferences/implications, if appropriate
• Comparison with any available prior ECGs; if none, so state. Comparative assessment is of major importance in clinical ECG interpretation and no reading is complete without this information.

Important Reminder: Computer-derived (electronic) interpretations of ECGs are subject to error and must be carefully reviewed, including the automated (electronic) measurements of intervals and of axis.
The ECG can also be affected by numerous artifacts and spurious findings, including lead reversals and misplacements, 60-Hz (or other electrical) interference, patient movement, poor electrode contact, and muscle tremor. The latter may simulate atrial flutter or fibrillation or sometimes ventricular tachycardia.
Note: For questions and answers relevant to this chapter, see Online Section 3: Quiz-Master.

Chapter 24: Limitations and Uses of the ECG

Review
Like most clinical tests, the electrocardiogram (ECG) yields both false-positive and false-negative diagnoses. For example, not all Q waves and not all ST segment elevations indicate myocardial infarction (MI) or ischemia and not all patients with actual MI show diagnostic ECG changes.
Clinicians must also be aware that a normal or nondiagnostic ECG also does not exclude left or right ventricular hypertrophy; intermittent, life-threatening brady-or tachyarrhythmias; acute pulmonary embolism; acute or chronic myopericarditis; and so forth.
Despite limitations in sensitivity and specificity, the ECG provides valuable, sometimes life-saving information in a wide range of clinical situations, including the evaluation of major medical syndromes such as syncope (fainting), coma, weakness, and hypotension/shock syndromes.

Chapter 24: Questions
1. Which classes of arrhythmias, and which specific arrhythmias, can lead to syncope (fainting) or near-syncope?

True or false (Questions 2 and 3):

2. A normal (“negative”) exercise tolerance test excludes clinically important coronary artery disease.
3. The more false-positive results associated with a particular test, the less sensitive the test is.
4. This ECG from a young adult man is consistent with which ONE of the following?
a. Right ventricular hypertrophy
b. Left–right arm lead reversal
c. Left posterior fascicular (hemi-) block
d. Myocardial infarction
e. Biventricular hypertrophy

5. Extra Credit!! What is the ECG diagnosis in this middle-aged man?

Chapter 24: Answers
1. Syncope (or near-syncope) can be caused or potentiated by a variety of bradyarrhythmias or tachyarrhythmias, including marked sinus bradycardia, actual sinus arrest, slow AV junctional escape rhythms, second- or third-degree AV block, atrial fibrillation or flutter with an excessively slow ventricular response, sustained ventricular tachycardia (monomorphic or polymorphic), paroxysmal supraventricular tachycardias, and atrial fibrillation or flutter with a very rapid ventricular response. The sudden spontaneous conversion from atrial fibrillation or flutter to sinus rhythm may be associated with prolonged pauses, sometimes sufficient to cause syncope. This type of “overdrive suppression” of the sinoatrial (SA) node constitutes an important example of the tachy-brady syndrome.
2. False
3. False. The sensitivity of a test is a measure of how well the test can detect an abnormality (e.g., coronary ischemia) in a given population. False-positive results (apparently abnormal results in the absence of the disease or syndrome in question) lower a test’s specificity, not its sensitivity. An example would be 1 to 2 mm of new horizontal or downsloping ST segment depressions during an exercise (stress) test in a young female subject without coronary artery disease risk factors.
4. b. Classic left–right arm lead reversal. The major clue is the combination of a negative P wave and negative QRS complex in lead I. The chest leads show a normal QRS pattern. To visualize a “corrected” ECG do the following: (1) take the negative of lead I (i.e., “flip” the polarity of all the waveforms) and (2) reverse the labels for leads II and III, and for leads aVR and aVL, respectively.
5. The ECG also shows left–right arm lead reversal. A “corrected” ECG with leads properly recorded is shown in this answer. The ECG shows sinus rhythm at about 80 beats/min with a borderline intraventricular conduction delay (QRS duration 100-110 msec). The PR interval is normal at about = 160 msec. Left atrial abnormality is present. The QT interval is within normal limits. Of most importance is definite evidence of a prior (indeterminate age) inferior Q wave MI, with pathologic Q waves in leads II, III, and aVF, and slight T wave inversions in those leads, consistent with ischemia. Nonspecific ST-T changes are present in lead V6. Could you have diagnosed the inferior MI despite the lead reversal? (See also Question/Answer 4.)

Chapter 25: ECG Differential Diagnoses: Instant Replays

See the text for an extensive list of electrocardiogram (ECG) differential diagnoses. Trainees and more seasoned clinicians alike should always have in mind a set of differential diagnoses for each apparent ECG finding. You should be able to say not only what you think the diagnosis is but also what other conditions could produce “look-alike” patterns. Then you should work to develop the critical thinking skills to articulate what line of reasoning supports your particular diagnosis, or why you cannot decide between certain possibilities.
For example, if your provisional diagnosis is an irregular-appearing narrow complex tachycardia, at a first level you should be able to state what the major differential diagnosis includes, namely: (1) artifact (e.g., due to Parkinsonian tremor); (2) atrial fibrillation; (3) sinus rhythm with frequent atrial ectopy; (4) atrial flutter with a variable response; or (5) multifocal atrial tachycardia (MAT).
A second level of differential diagnosis is related to possible causative or contributory factors. With atrial fibrillation, these factors would include hypertension, advanced age, valvular heart disease, cardiac surgery, coronary disease, cardiomyopathy, hyperthyroidism, and severe obstructive sleep apnea/obesity, among many others
At a third and deeper level is an understanding of the actual or putative electrophysiologic mechanisms of the ECG findings so that you are not solely engaging in “pattern” recognition and creating lists of causes. For example, for atrial fibrillation, basic mechanisms involve increased automaticity in the area of the pulmonary vein orifices and multiple microreentrant circuits in the atria. The role of other factors in the pathogenesis of atrial fibrillation (anatomic, genomic, and neuroautonomic) is a major area of contemporary cardiologic investigation.
This multilayered approach to ECG analysis is essential in helping to determine what therapeutic modality you should choose and to be aware of all of the available options and their potential side effects and complications.
Never be afraid to say, “I am not sure,” or to state the major finding(s) and offer a provisional differential diagnosis. Also, recognize when you may need more information to make a diagnosis. Finally, remember the importance of serial (and prior) ECGs and of obtaining more extended rhythm strips and serial ECGs when questions remain about the mechanism of an arrhythmia or about possible evolving ischemia, respectively.

Chapter 25: Questions and Answers
See online quizzes (Section 3: Quiz Master) and go to the free ECG Wave-Maven site (https://ecg.bidmc.harvard.edu) for a collection of over 500 tracings with answers, ranging in difficulty from entry level to advanced.