General

Readers interested in understanding more about the underpinnings of electrocardiogram (ECG) interpretation should refer to the series of six scientific statements included in the Recommendations for the Standardization and Interpretation of the Electrocardiogram. These landmark articles, written under the auspices of the major cardiology societies, are highly recommended to students and experts alike.
The full texts are freely available at societies’ websites, including via the following links to the American College of Cardiology:

Part I: The Electrocardiogram and Its Technology
http://content.onlinejacc.org/cgi/content/full/49/10/1109
Part II: Electrocardiography Diagnostic Statement List
http://content.onlinejacc.org/cgi/reprint/49/10/1128.pdf
Part III: Intraventricular Conduction Disturbances
content.onlinejacc.org/cgi/content/full/53/11/976
Part IV: The ST Segment, T and U Waves, and the QT Interval
content.onlinejacc.org/cgi/reprint/53/11/1003.pdf
Part V: Electrocardiogram Changes Associated with Cardiac Chamber Hypertrophy
content.onlinejacc.org/cgi/reprint/53/11/992.pdf
Part VI: Acute Ischemia/Infarction
content.onlinejacc.org/cgi/reprint/53/11/1003.pdf

Supplement to Chapters 1 to 6

Basic Cardiac Electrophysiology: Mini-Review
This book is devoted to describing the ECG, an invaluable tool in clinical technology that provides essential information about the status of the cardiac rhythm and the effects of certain major abnormalities, including ischemia and infarction, cardiac chamber enlargement, drug toxicity, and life-threatening metabolic disturbances (e.g., severe hyperkalemia). We also emphasize important limitations of the ECG.
Clinicians should be aware that the surface ECG waveforms (as recorded on the usual 12 leads or selected monitor leads) represent the summation of electrical activity generated by enormous numbers of individual cardiac cells (myocytes) in the atria and ventricles. However, the inherent electrical activity of the sinus node, the atrioventricular (AV) node, and the His–Purkinje network (intrinsic pacemakers and specialized conduction system) are not directly recorded. Fortunately, “hidden information” about their normal or abnormal function can often be inferred from the ECG.
As an example, a wide QRS complex may indicate a block in one of the bundle branches. The morphology usually indicates whether the block is in the right or left bundle branch (Chapter 8). Further, as discussed in Chapter 17, sometimes the key distinction between a nodal versus infranodal location of AV blocks can be made from the surface ECG.
Understanding of the basis of the surface ECG is facilitated by some knowledge about the electrical properties of individual cardiac cells themselves. This subject is one of enormous complexity and ongoing research.
The intent of the following brief section, therefore, is to outline some basic aspects of cardiac electrophysiology. The emphasis is on the action potential, the fundamental electrical cycle of single myocardial cells as they depolarize (activate or discharge) and repolarize (recover or recharge). Readers interested in a more in-depth understanding can refer to the Bibliography.

The Heart as an Electrically Excitable Medium
The heart is an example of a biologically excitable medium. Other examples include the nervous system, the bowel, and the muscular system. Electrically excitable media are capable of propagating waves but also have a refractory period when they cannot be excited.
The electrical excitability of the heart (Figs. S2.1 and S2.3) depends on the facts that normal cardiac cells:

(1) are polarized (charged) under resting conditions, that is, there is a transmembrane potential gradient;
(2) are capable of rapidly discharging (depolarizing) and then more gradually recharging (repolarizing);
(3) can conduct (propagate) electrical currents; and
(4) include specialized cell groups, in particular those constituting the sinus (sinoatrial [SA]) node, that depolarize and repolarize automatically such that one activation–recovery cycle is followed by another and another, and so on. The specialized pacemaker cells possess inherent automaticity that is responsible for reliably maintaining and tuning the rhythmicity of the heart over the full range of physiologic states. Other cardiac cells outside the sinus node (e.g., in the atria and ventricles) have some degree of automaticity. However, their activation usually requires stimulation by neighboring cells and the initiating stimulus for each normal heartbeat starts in the sinus node. The automaticity of the sinus and AV nodes, in turn, are importantly modulated by the autonomic nervous system (sympathetic and parasympathetic branches).

Transmembrane Potential (Voltage) Differences (Gradients)
The polarization of cardiac cells is such that under resting conditions they carry a negative charge on the inside of the cell membrane relative to the outside of the membrane. This transmembrane potential difference is importantly related to the fact that cardiac cell membranes are semipermeable. Under resting conditions, the membrane selectively permits only one species of ion, namely potassium (K+), to cross freely, while the membrane is relatively impermeable to other ions, notably sodium (Na+) and calcium (Ca2+). Consequently, under resting (baseline) conditions the cells accumulate a predominance of K+ ions inside relative to outside, along with a predominance of Na+ and Ca2+ ions outside relative to inside. The exquisitely coordinated, energy-requiring mechanisms for creating these ionic imbalances are complex. They involve a special inward K+ current as well as ion exchangers and ion pumps located within the membrane.
During resting conditions of cardiac cells, the tendency of intracellular K+ ions to move down their concentration gradient toward the outside of the cell is counterbalanced by the “pull” of negatively charged ions (e.g., phosphate) inside the cell that are too big to cross through the membrane. This dynamic “push–pull” process leads to the negative/positive relationship (polarization) of the inside of the cells relative to the outside, creating the nonzero “equilibrium” potential.

The Action Potential: Key to the Heart’s Electrical Properties
Electrical stimulation perturbs this equilibrium and leads to depolarization and then repolarization associated with the opening and closing of specialized ion channels along the membrane. The channels act like mini-gatekeepers. These currents that result from movements of ions, in turn, produce changes in the transmembrane potential.
When the sequential changes in intracellular voltage of a single heart muscle cell (fiber) are graphed as a function of time, the result is a two-dimensional depiction of the action potential. In contrast, the ECG represents the changes in extracellular potentials of myriads of cells as a function of time. Despite fundamental differences, the intracellular action potential of individual cells (especially ventricular cells) bears important correspondences with the surface QRS-ST-T sequence recorded by the ECG (Fig. S2.1).

Fig. S2.1 The intracellular recording of a single ventricular cell (fiber), the action potential (AP), is plotted above a simultaneous ECG, the surface recording from the entire heart. Phase 0 of the AP corresponds to the rapid upstroke of the QRS, phase 2 to the ST segment, and phase 3 to inscription of the T wave.

All electrically excitable cells have a distinct pattern to their action potential, and the cardiac cell is no exception. We will begin by focusing on the action potential of the ventricles (and Purkinje fibers) as a model. Although we usually think of the activity of ventricles in three sequential stages—resting state, depolarization, and repolarization—the action potential that underlies these stages is actually divided into five phases, denoted as phases 0 through 4, that include these three major states (Fig. S2.2).

Fig. S2.2 Highly simplified schematic showing the five phases of the action potential and some of the major ionic mechanisms.

By convention, depolarization of the ventricles is termed phase 0. This initial phase is caused by the opening of Na+ channels along the cell membrane. Owing to the electrochemical gradient, there is an initial influx of positively charged Na+ ions into the cell, which has a negative intracellular charge and a relatively lower concentration of Na+ ions. Once a threshold potential (about −50 millivolts [mV] in ventricular cells) is reached, the cells rapidly depolarize as the Na+ channels fully open. Overall, transmembrane voltage (inside vs. outside of the cells) therefore quickly changes from approximately −90 mV to approximately +10 mV.
The cardiac electrical system can be considered as a complex network. Cardiac cells are interconnected by specialized links, called gap junctions. These connections facilitate electrical communication between the myofibers.
Phase 0 of the action potential, representing ventricular depolarization, coincides with the rapid upstroke of the QRS complex of the surface ECG. Not surprisingly, factors that directly impair opening of Na+ channels, including certain drugs and hyperkalemia, tend to widen the QRS complex and slow ventricular conduction.
Phases 1 to 3 represent ventricular repolarization, during which time the ventricular myocytes begin to lose their positive charge.
Phase 1 marks the end of phase 0—specifically, the inactivation of the Na+ channels, causing a cessation of Na+ influx. (There is a slight notch caused by a transient loss of positive voltage because of the outflow of K+ ions.)
Phase 2 of the ventricular action potential is called the plateau phase, during which there is stability of the transmembrane potential. This phase is created by the balance between the inflow and outflow of two positively charged particles, Ca2+ and K+, respectively.
The plateau phase is unique to the cardiac action potentials of ventricular myocytes (vs. central and peripheral nerves) and is responsible for the relatively prolonged duration of the cardiac myocyte electrical cycle. Of note, during phases 1 and 2 (and the early part of phase 3), the ventricular myocyte is normally incapable of being depolarized again—that is, it is refractory to activation by electrical stimuli.
Of key importance is the entry of Ca2+ ions during the action potential and the release of Ca2+ ions within the working heart muscle cells, causing contraction (shortening) of these cells. This process of electromechanical coupling links the electrical events with the pumping function of the heart.
During phase 3, Ca2+ channels close, shutting off the inflow of the positive Ca2+ current, leaving the efflux of positively charged K+ current unopposed. This drives the transmembrane potential back down toward its resting level of −90 mV.
Phase 4 of the ventricular action potential marks the return to the resting phase.
Fig. S2.3 shows the relationship of all four phases of the ventricular myocyte action potential to the surface ECG complex.

• Phase 0 to 1 corresponds to the QRS complex.
• Phase 2 of the ventricular action potential corresponds to the ST segment. During this phase, the ECG begins to return to baseline because there is no net current flow between cells, which are all at about the same potential.
• Note: Factors that prolong phase 2, such as hypocalcemia and certain drugs, will prolong the ST segment component of the QT interval. Factors such as hypercalcemia or digoxin, which shorten phase 2 of ventricular action potentials, will tend to abbreviate the ST segment phase of the ECG.
• Phase 3, which occurs at somewhat different times in different parts of the ventricular myocardium, corresponds with inscription of the T wave.
• Phase 4 corresponds to the T-Q segment (used as isoelectric baseline of the standard ECG).

Fig. S2.3 Comparison of action potentials of ventricular, atrial, and sinus node cells. Note the shorter duration of the latter, along with its spontaneous phase 4 depolarization.

Atrial muscle cells have action potentials that resemble ventricular ones but the atrial action potentials are shorter in duration (see Fig. S2.3).

Sinus and AV Nodal Action Potentials
Cells in the sinoatrial (SA) node (Fig. S2.3) and AV node have markedly different action potentials from those in atrial and ventricular/Purkinje fibers, which we have been describing up to now. First, the depolarization in these nodal cells is much slower than the rapid phase 0 depolarization in the ventricular cells, and is driven primarily by the “slow current” rather than “rapid” Na+ current. Second, the resting membrane potential is not relatively constant but has a spontaneous drift toward depolarization, such that the cells generate action potentials in an automated way. This spontaneous depolarization is what accounts for the inherent automaticity of the sinus node. The ionic basis of spontaneous depolarization and “pacemaker” currents is a subject of active study. The slow entry of Na+ ions (“funny current”) seems to play an important role.
See http://circ.ahajournals.org/content/115/14/1921.full for a concise review of sinus node function.
Because the spontaneous rate of sinus node cells is relatively faster than that of other pacemaker cells (e.g., in the AV node area) and elsewhere, the sinus node normally dominates the initiation of the heartbeat. Other pacemakers can take over (escape rhythms) if the sinus node fails and sometimes with abnormal conditions that increase the automaticity of cells in other parts of the heart (e.g., the atria, AV junction, or ventricular conduction system). This abnormal automaticity is one mechanism for premature ectopic beats and for some types of tachycardias.
The pacemaker cells do not conduct impulses rapidly, compared with atrial and ventricular cells. Indeed, slow conduction of current across the AV node accounts for most of the PR interval on the ECG, a physiologic delay that allows the ventricles time to fill with blood after atrial contraction and before ventricular contraction.
Finally, it is important to emphasize that the activities of the sinus and AV nodes are importantly influenced by the autonomic nervous system and by certain drugs. For example, increased vagal tone and adenosine both make the resting transmembrane potential of these pacemaker cells more negative, thus decreasing their rate of depolarization and slowing the heart rate and increasing the PR interval. Decreases in vagal (parasympathetic) tone and increases in sympathetic tone have the opposite effect. The autonomic nervous system also effects working cardiac fibers. For examples, the strength (inotropic state) of atrial and ventricular muscle is increased by increased sympathetic (adrenergic) stimulation.

Intracardiac Recordings
The surface ECG, despite its remarkable utility, does not directly record certain essential physiologic events. However, some of these events can be recorded using specialized systems of electrodes positioned within the heart during invasive cardiac electrophysiologic studies (EPS), as shown in Fig. S2.4.

Fig. S2.4 A typical diagnostic cardiac EP study involves placing recording catheters inside the heart, usually through the femoral vein(s), designated as follows: HRA, High right atrium (close to the sinus node); His, across the tricuspid valve to record the local atrial signal (A), His bundle potential (H), and right ventricular outflow tract (V) electrograms; RVA, right ventricular apex electrogram. A–H and H–V intervals, measured from the His catheter recording, represent conduction time through the AV node and His–Purkinje system, respectively. Normal values: A–H: 50 to 120 msec; H–V: 35 to 55 msec. (Another catheter, not shown, is placed in the coronary sinus.)

These intracardiac recordings show that the PR interval normally comprises three sequential subintervals. The first interval (HRA–A, or P-A interval) is due to conduction of the signal from the sinus node in the high right atrium (HRA) through atrial tissue to the AV node. The second one (A–H, usually accounting for the majority of the PR interval on the surface ECG) reflects conduction time through the AV nodal tissue to the bundle of His. The third interval (H–V) represents relatively rapid conduction through the His bundle, the bundle branches, and Purkinje fibers into the ventricles.
These subintervals can be recorded with electrical catheters positioned (1) in the high right atrium (close to the sinus node) and (2) across the tricuspid valve (at the area of AV node, His bundle, and right ventricle).
Visualization of A–H (AV nodal conduction) and H–V (His bundle, or infranodal conduction) intervals is important (see Chapter 17) in discrimination of AV delays and second-degree AV blocks into nodal and infranodal types. Infranodal blocks are of particular concern and often require the implantation of a permanent pacemaker. In contrast, prolongation of the PR interval or second-degree AV heart block because of nodal disease is usually not of imminent concern, unless associated with major symptoms (see Chapter 17).
Invasive EP studies, as discussed in the text, are also essential in localizing the site(s) of supraventricular and ventricular arrhythmias and in therapeutic interventions using radiofrequency ablation (and other ablation modalities such as cryo- and laser technology). These modalities are used to treat a wide range of tachyarrhythmias, including various types of paroxysmal supraventricular tachycardia (PSVT), atrial flutter, atrial fibrillation, and certain types of ventricular tachycardias.

Supplement to Chapters 7 and 8

How Do You Measure the Mean QRS Axis with a Bundle Branch Block?
The mean QRS axis in the frontal plan (QRS axis) is routinely measured from 12-lead ECGs. However, no formal guidelines are given for how to operationally measure the axis when the QRS is widened by a bundle branch block, especially right bundle branch block (RBBB). The prolonged terminal part of the QRS in RBBB reflects delays in right ventricular activation; axis determination is primarily of importance in diagnosing left anterior or left posterior fascicular block. Therefore, a reasonable approach is to estimate the mean frontal plane QRS axis using just the first 80 to 100 msec of the QRS (reflecting activation of the left ventricle). For left bundle branch block and other intraventricular conduction delays (IVCDs), the entire QRS can be used or just the initial 80 to 100 msec. The results will usually be comparable. The challenge of measuring axis with a wide QRS using different parts of the QRS complex is one that could be studied in further detail with contemporary digital recordings and large databases.

What Are the Cutoff Thresholds for Left Anterior Fascicular and Left Posterior Fascicular Blocks?
Confusion and inter-observer variability may arise because different sources and different authors have made different recommendations. The formal threshold for left anterior fascicular block (LAFB) is classically set at −45° not −30°, the latter being the cutoff for left axis deviation. LAFB, by itself, may widen the QRS slightly but usually not beyond 110 to 120 msec. Most cases of pure LAFB are associated with small r waves in the inferior leads and a small q wave in lead aVL (and often lead I). In addition, because the vector loop in LAFB goes in a counterclockwise direction (inferior to superior), the peak of the R wave in aVL will occur just before that in lead aVR. When LAFB and inferior wall myocardial infarction (MI) coexist, leads II, III, and aVF may show frank QS waves, not rS waves, or sometimes they show very small, notched r waves. A QR complex in the inferior leads is not consistent with LAFB because it indicates that the inferior forces are oriented inferiorly and rightward, whereas with LAFB they are oriented leftward and superiorly.
LAFB, because of the posteroinferior orientation of the initial QRS vector, is also often associated with two subtle changes in the precordial QRS complex: (1) Initial r wave progression may be slow with micro q waves (about 10-20 msec in duration) in leads V1 and V2. (2) Small s waves are usually seen in the lateral chest leads.
LAFB is one of the most common causes of left axis deviation. In contrast, left posterior fascicular block (LPFB) is one of the least common causes of right axis deviation. Indeed, the latter diagnosis requires excluding left–right arm electrode reversal, normal variants (especially in young adults), rightward mediastinal shift changes in cardiac position, right ventricular overload syndromes (e.g., acute pulmonary embolism, chronic thromboembolic pulmonary hypertension, severe pneumonitis, obstructive or restrictive pulmonary disease), and lateral wall MI (because of loss of lateral QRS forces). In the literature, the frontal plane axis threshold for diagnosing LPFB is variously given between +100° and +120°. Of note, in almost all cases, LPFB accompanies RBBB as part of so-called bifascicular block. The frontal plane leads are often configured in the opposite fashion compared to LAFB—specifically, rS complexes in I and aVL and qR complexes inferiorly. Seeing isolated LPFB is extremely rare; if you are making this diagnosis more than once or twice a year, you have an unusual practice or you are mistaking other, much more common causes of isolated right axis deviation for LPFB.

RBBB with Right Axis Deviation
Finally, to complete this section, we note that there are three major causes in adults (excluding left–right arm limb lead reversal with RBBB) of the combination RBBB and right axis deviation: (1) right ventricular overload syndrome (with pressure or volume overloads); (2) lateral wall MI with RBBB; and (3) RBBB and LPFB (a form of bifascicular block).

Bundle Branch Block vs. “Bundle Branch Block Plus”
When you encounter an ECG with an RBBB or LBBB pattern you should make it a habit of looking for signs of additional abnormalities. Ask yourself: Is this ECG consistent with a “pure” BBB pattern or does it raise consideration of additional abnormalities (for which we use the informal term “BBB plus”)?
A “pure BBB” here refers to an RBBB or LBBB pattern with the expected secondary ST-T changes. “BBB plus” would include, but is not limited to, evidence of one or more of the following in concert with the QRS morphology consistent with right or left bundle branch block:

1. Ischemic-appearing ST-T changes
2. Q waves consistent with prior infarction
3. Prominent QT(U) prolongation
4. Chamber hypertrophy/overload
5. QRS axis deviation
6. Extreme widening of the QRS (e.g., 170-180 msec or more), suggesting marked ventricular scarring, hyperkalemia, or drug toxicity (Na+ channel blockers)
7. Prominent notching or fragmentation of the QRS complex. For example, notching of the ascending limb of an rS (or QS) wave in the mid-precordial leads with LBBB has been reported as a relatively specific but not sensitive marker of underlying infarction (sometimes referred to as Cabrera’s sign).

An example of “LBBB plus” is shown in Fig. S2.5.

Fig. S2.5 Left bundle branch block (LBBB) “plus” pattern from a 79-year-old woman with ischemic cardiomyopathy, status post multiple revascularization procedures. In addition to the classic LBBB morphology are the findings of sinus rhythm with (1) left axis deviation; (2) very wide QRS interval (∼200 msec); (3) notched and fragmented QRS; (4) ST elevations with T wave inversions in V3 and V4; and (5) marked left atrial abnormality (very broad, low amplitude terminal P wave in V1).

Keep in mind that BBB, especially LBBB, may both mask and mimic the findings of acute or chronic MI. With LBBB, ST elevations in leads with predominant R waves or ST depressions (or T wave inversions) in leads with predominant rS or QS waves should raise strong consideration of ischemia/infarction. Slow or even absent r wave progression in the right to mid-precordial leads is an expected feature of LBBB. However, a QR pattern (with a Q wave of 40 msec or more in duration) in one or more of leads I, V4 to V6, II, and aVF raises consideration of underlying infarction.
BBB patterns are anticipated to prolong the QT/QTc since the latter interval includes the QRS duration. However, marked QT prolongation and/or prominent U waves should raise consideration of superimposed drug effect or hypokalemia.
The presence of left atrial abnormality in concert with LBBB or RBBB makes underlying left ventricular hypertrophy more likely. The already low sensitivity of voltage criteria for LVH in middle-aged to older adults may be further reduced by RBBB because of decreased amplitude of S waves in leads V1 and V2.
We discussed the differential diagnosis of RBBB with right axis deviation previously. There has been debate in the literature about the implications of LBBB with left axis deviation (LAD), defined as a mean frontal plane QRS axis of −30 degrees or more negative. Overall, patients with LBBB and LAD have more severe structural heart disease than those with a normal axis. However, recall that LBBB, by itself, is usually a marker of underlying organic heart disease.

Supplement to Chapters 9 and 10: Acute Myocardial Ischemia and Infarction

These tandem chapters describe some of the patterns that may simulate the ST elevations because of myocardial ischemia or infarction (see also Chapter 25). One of these patterns that may mimic ischemia is referred to most commonly as the “early repolarization pattern.” This term most often is used to describe ST elevations seen in healthy subjects and also referred to as “benign ST elevations” or benign early repolarization. For those interested, the literature contains some controversy about whether early repolarization is a normal benign finding or whether it sometimes may be a marker of susceptibility to potentially lethal ventricular arrhythmias in a subset or subsets of individuals. Clearly, for the vast majority of subjects with this finding (usually healthy young adults with increased cardiac vagal tone), the finding is indeed benign and likely a marker of physiologic heterogeneities in ventricular repolarization times. Whether a similar ECG phenotype may have pathologic implications in certain individuals (“malignant early repolarization” pattern) is an active topic of discussion in the literature.

Supplement to Chapter 13: Sinus and Escape Rhythms

Sinus Tachycardia: More Detailed Classification
Sinus rhythm (rate ≥100 beats/min) is not a primary arrhythmia in the usual sense (with the extremely rare exception of sinus node reentrant tachycardia). Instead, sinus tachycardia, in the vast majority of healthy subjects and those with pathology, occurs in the context of increased sympathetic and decreased parasympathetic tone as part of the body’s autoregulatory responses to meeting increased metabolic needs. Sinus tachycardia is an expected and appropriate finding in the context of increased activity (e.g., climbing a few flights of stairs, running for a bus, or during exercise). It is also important in the setting of multiple pathologic states where increased cardiac output is required. A relatively small but very interesting subset of subjects has sinus tachycardia that does not appear to be commensurate with increased systemic needs for augmented cardiac output. Sinus tachycardia in these cases can be considered as inappropriate.
Based on these considerations, sinus tachycardia can be considered in two major classes:

I. Sinus tachycardia: Appropriate
A. Physiologic settings: in fetuses and neonates; on children or adults during and just after exercise, or with emotional stress
B. Pathologic conditions associated with increased sympathetic and decreased vagal tone at rest, for example heart failure; fever/sepsis; hyperthyroidism; pulmonary embolism; severe anemia; pain; volume loss (dehydration; intravascular blood loss); hypoglycemia; hypoxemia; pneumothorax; pericardial tamponade, pheochromocytoma, etc.
C. Pharmacologic or substance-related, for example vagolytic (anticholinergic) or sympathomimetic drugs; abrupt beta-blocker withdrawal; caffeine; alcohol excess or withdrawal; cocaine; opioid withdrawal, monoamine oxidase inhibitor (MAOI) syndrome, etc.
II. Sinus tachycardia: Inappropriate
A. Idiopathic sinus tachycardia (IST) syndrome
B. Postural (orthostatic) tachycardia syndrome (POTS)
C. SA node reentrant tachycardia (SANRT)
D. Post-COVID-19 (“long-COVID” syndrome)

Prominent sustained sinus tachycardia at rest in adults is often an ominous finding because of its association with the pathologic conditions listed previously, under point IB. For example, unexplained sinus tachycardia may be a major clue to acute or chronic volume loss, severe pulmonary disease, infection, and so forth. The higher the rate, the more severe the pathologic derangement is likely to be, due to autonomic activation. In most cases, resting sinus tachycardia has a traceable cause and may be the first clue to a life-threatening abnormality.
Postural (orthostatic) tachycardia syndrome (POTS) has some similarities to IST. But the former is defined in adults by an increase in the heart rate (HR) ≥30 bpm (or ≥40 bpm in adolescents) for more than 30 seconds upon standing from a recumbent position. Of importance is the absence of orthostatic hypotension (≥20 mm Hg drop in systolic blood pressure).
Patients with POTS are symptomatic. Subjects complain of lightheadedness, occasional syncope, anxiety, and fatigue with standing that is relieved by recumbence. POTS has been attributed to abnormal autonomic function and possibly an autoimmune diathesis, but its basic mechanism(s) and biomarkers remain to be defined.
The COVID-19 pandemic has led to recognition of a so-called long-COVID condition. The syndrome, usually noted weeks or longer after viral infection, is characterized by dizziness, chest discomfort, and shortness of breath. Inappropriate tachycardia may be present. Similarities to POTS have raised the question of common pathogenetic mechanisms.
Finally, a clinically rare type of inappropriate sinus tachycardia has been attributed to a reentrant supraventricular tachycardia,4 involving the SA node itself (acronymically called SANRT). The rhythm most closely resembles a right atrial tachycardia. Unlike other causes of appropriate or inappropriate sinus tachycardia, SANRT should start and stop abruptly. Much more commonly recognized types of supraventricular reentrant tachycardias, which involve the AV not the SA node, are discussed in Chapters 14 and 19.
Readers interested in these more advanced topics (usually relevant to puzzling patients who have had multiple referrals for unexplained sinus tachycardia) are referred to an extensive bibliography on the subject of inappropriate sinus tachycardias, with some references given here.

Selected References
(1) Grubb, B. P. (2008). Postural tachycardia syndrome. Circulation, 117, 2814–2817.
(2) Olshanksy, B., & Sullivan, R. M. (2019). Inappropriate sinus tachycardia. Europace, 21, 194–207.
(3) Raj, S. T. (2013). Postural tachycardia syndrome (POTS). Circulation, 127, 2336–2342.
(4) Yusuf. S., & Camm, A. J. (2005). Deciphering the tachycardias. Clin Cardiol, 28, 267–276.
(5) Sheldon, R.S., et al. 2015 Heart Rhythm Society Expert Consensus Statement on the Diagnosis and Treatment of Postural Tachycardia Syndrome, Inappropriate sinus tachycardia, and Vasovagal Syncope. Heart Rhythm 2015, 12:e41-63.
(6) Raj, S. R., Arnold, A. C., Barboi, A., et al. (2021). Long-COVID postural tachycardia syndrome: an American Autonomic Society statement. Clin Auton Res, 31, 365–368. https://doi.org/10.1007/s10286-021-00798-2
(7) Miglis, M. G., Larsen, N., & Muppidi, S. (2022). Inappropriate sinus tachycardia in long-COVID and other updates on recent autonomic research. Clin Auton Res. https://doi.org/10.1007/s10286-022-00854-5
(8) Ali, M., Haji, A. Q., Kichloo, A., Grubb, B. P., & Kanjwal, K. (2021). Inappropriate sinus tachycardia: a review. Rev Cardiovasc Med, 22, 1331–1339. https://doi.org/10.31083/j.rcm2204139

Heart Rate variability and Autonomic Tone
The widely used term “regular sinus rhythm” is a misnomer. Sinus rhythm in healthy subjects shows a considerable beat-to-beat variability. These fluctuations, although not readily perceptible to the individual, are clearly evident on graphical displays of beat-to-beat changes in sinus RR intervals (termed NN intervals). Graphs of instantaneous heart rate (or cardiac interbeat intervals) on the y-axis versus time on the x-axis are called heart rate time series plots. An example is shown in Fig. S2.6.

Fig. S2.6 Heart rate time series graph (over 6 minutes) obtained from the Holter monitor recording of a healthy young adult during daytime. The ECG showed sinus rhythm. Note the complex fluctuations in rate on a beat-to-beat basis. The inset shows a magnification of one minute of data. The oscillations in heart rate (about 16/min) exemplify respiratory sinus arrhythmia. Heart rate goes up with inspiration and down with expiration under physiologic conditions because of vagal tone modulation of the sinus node. bpm, beats per minute.

The most important source of physiologic short-term heart rate variability (HRV) (i.e., occurring over seconds or less) is respiration. As we breathe in, our heart rate increases and as we breathe out, our heart rate decreases. (As a mnemonic aid: inspiration → increase.) You can test for these effects by feeling your pulse while breathing slowly and deeply. If you are wearing a portable heart monitor, you can see the changes reflected in the pulse rate display. These variations are mediated primarily by the vagus nerve and are most pronounced in young healthy individuals and athletes. Aging, disease, and anticholinergic medications reduce the degree of physiologic respiratory sinus arrhythmia (RSA). Indeed, the term arrhythmia is another misnomer because this type of variability reflects healthy cardioautonomic function. The term “arrhythmia” implies an abnormality.
RSA is also referred to as high frequency HRV because the fluctuations track respiration, which usually occurs at a frequency between 0.15 and 0.40 Hz (Hertz = cycles per second) in adults at rest or with moderate activity. This frequency band is equivalent to breathing at a rate of 9 to 24/min. As noted, these high-frequency, high-rate fluctuations are attributable to vagal tone modulation. Lower-frequency fluctuations in heart rate are also important and are attributable to both parasympathetic and sympathetic influences, as well as nonautonomic factors.
The analysis of HRV has engendered considerable interest, with thousands of publications over the past decades. At present in the United States, this type of analysis is primarily used for research purposes. HRV may also be employed in clinical autonomic testing. One example of a promising translational application is in the early detection of neonatal sepsis.1

The classic and still relevant 1996 Circulation article by the Task Force of the European Society of Cardiology and the North American Society of Pacing Electrophysiology that describes many of these methods and their scientific background is available at:

http://circ.ahajournals.org/content/93/5/1043.full

More recently, a new approach to the analysis of heart rate dynamics, termed heart rate fragmentation, has been proposed to detect and quantify the breakdown of short-term (vagal) neuroautonomic regulation of sinus node function, most relevant in aging and with cardiac disease. This approach appears to have value in prediction of major adverse cardiovascular events, including atrial fibrillation, and overcomes salient limitations of traditional algorithms for assessing vagally mediated fluctuations in beat-to-beat cardiac interval dynamics.(2–4)

Selected References
(1) Sullivan, B. A., Grice, S. M., Lake, D. E., et al. (2014). Infection and other clinical correlates of abnormal heart rate characteristics in preterm infants. J Pediatr, 164, 775–780.
(2) Costa, M. D., Davis, R. B., & Goldberger, A. L. (2017). Heart rate fragmentation: A new approach to the analysis of cardiac interbeat interval dynamics. Front Physiol, 8, 255. http://doi.org/10.3389/fphys.2017.00255
(3) Costa, M. D., Redline, S., Davis, R. B., Heckbert, S. R., Soliman, E. Z., & Goldberger, A. L. (2018). Heart rate fragmentation as a novel biomarker of adverse cardiovascular events: The Multi-Ethnic Study of Atherosclerosis. Front Physiol, 9, 1117. http://doi.org/10.3389/fphys.2018.01117
(4) Costa, M. D., Redline, S., Soliman, E. Z., Goldberger, A. L., & Heckbert, S. R. (2021). Fragmented sinoatrial dynamics in the prediction of atrial fibrillation: The Multi-Ethnic Study of Atherosclerosis. Am J Physiol Heart Circ Physiol., 320, H256, http://doi.org/10.1152/ajpheart00421.2020

Supplement to Chapters 14 and 15

Readers are encouraged to review the 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients with Supraventricular Tachycardia. This statement is available at each of the societies’ respective websites, including:

http://content.onlinejacc.org/article.aspx?articleid=2443667

Readers should always check for the latest updates of these and other guideline statements issued by the major cardiology societies in the United States and Europe.

Short vs. Long RP Tachycardias
Some clinicians classify supraventricular tachycardias (SVTs) into those with “short” versus “long” RP intervals. The authors of this text do not favor using this schema in differential diagnosis because it can be more confusing than helpful for a number of reasons: (1) None of the classifications into “short” and “long” RP variants provides definitive mechanistic information. For instance, a suggested classification is based on the ratio of the RP/PR (≤1 for short and >1 for long RP variants). However, this categorization only applies if the P waves are ectopic and, preferably, retrograde (negative in lead II). (2) In a large percentage of cases of AV nodal reentrant tachycardia (AVNRT), the retrograde P waves are “buried” in the QRS so the ratio is not meaningful. (3) In other cases, the P waves may be hard to identify, making it impossible to tell if the SVT is short or long RP in nature. (4) A short RP may be seen with AVNRT, atrioventricular reentrant tachycardia (AVRT) or atrial tachycardia (AT). (5) A long RP tachycardia may be seen with AVRT with a slowly conducting bypass tract, with atypical forms of AVNRT, or in some cases of AT.

On Reporting the Ventricular Rate in Atrial Fibrillation (AF)
The ventricular response in atrial fibrillation (AF) is almost invariably reported as a mean value (usually over 10 sec based on the standard ECG read-out, which is 10 sec in length). A more complete and rigorous report would be to note that the rate is based on the patient being at rest and to give the range of values (lowest to highest). An example is shown in Fig. S2.7.

Fig. S2.7 This ECG obtained at rest shows atrial fibrillation with a rapid ventricular response, mean rate of 120 beats/min, with a wide range of instantaneous rates. Note: the instantaneous rate is computed by the simple algorithm of dividing 1,500 by the number of small boxes between consecutive QRS complexes (see Chapter 3). In this case the denominator ranges between 23 and 10, to yield 65 and 150 beats/min, respectively, as the minimum and maximum beat-to-beat rates for this 10 second sampling period.

This expanded way of describing the rate in AF (giving not just the mean rate but the range, with the indication of resting or nonresting status, along with the relevant drugs the patient is taking) is clinically useful. The ventricular response in AF is usually quite unstable such that even low levels of activity may cause substantial increases in the ventricular rate. Sustained high rates in AF may lead to further deterioration of ventricular function as part of the tachy-cardiomyopathy syndrome.
Trainees should also be aware that the frequently posed question “What is the rate?” in cases of AF is not, as the mathematicians might say, “well-posed.” Obviously, the rate being referred to in the parlance of the wards is the ventricular rate. But in many cardiac arrhythmias, two different rates are present: atrial versus ventricular. In AF, for example, the atrial rate is usually too fast to count from the surface ECG (350-600 cycles/min) and represents an electrical depolarization rate, not a mechanical (beat or pulse) rate. Different atrial and ventricular electrical rates are also observed in sinus rhythm with second- or third-degree AV block; atrial tachycardia with block and atrial flutter; and cases of ventricular tachycardia with AV dissociation.

Atrial Fibrillation (AF) and the Pulse Deficit Phenomenon
AF is one of the arrhythmias often associated with a pulse deficit. This term, relevant to bedside physical diagnosis, applies when the QRS rate is noticeably greater than the palpated pulse rate. The explanation is that with very rapid rates in AF (or with very early cycle premature ventricular complexes [PVCs]), each depolarization may not be capable of producing enough of a cardiac output (strong enough left ventricular contraction) to generate a detectable pulse. Therefore, the radial or carotid pulse rates, especially, may underestimate the actual ECG rate. The same phenomenon can occur with premature atrial contractions. Students should not confuse pulse deficit with pulsus alternans in heart failure syndromes or pulsus paradoxicus in pericardial (cardiac) tamponade.

Supplement to Chapter 16

A 2017 Task Force of the American Heart Association, the American College of Cardiology, and the Heart Rhythm Society have jointly issued guidelines on “Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death.”

https://www.ahajournals.org/doi/epub/10.1161/CIR.0000000000000549

Readers should check for updates of this and other society guidelines and recommendations as they become available on this and other ECG/arrhythmia topics.

Supplement to Chapter 19

Some bradycardias associated with sinus node disease may be difficult to classify precisely. Fig. S2.8 shows the ECG from an older adult woman with severe bradycardia that persisted even after discontinuing digoxin, used in the context of heart failure with a reduced left ventricular ejection fraction.

Fig. S2.8 ECG rhythm strip from a patient with severe bradycardia and supraventricular escape beats, sometimes referred to as escape bigeminy. See text for details.

The lead II rhythm strip shows an ectopic atrial rhythm with atrial bigeminy and intermittent ectopic atrial and junctional (nodal) beats. This pattern is sometimes termed “escape bigeminy.” Paroxysmal AF was noted at other times. The patient required a pacemaker for “sick sinus syndrome.”

Supplement to Chapter 21

The 2015 American Heart Association Guidelines for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiac Care are provided at:

https://www.ahajournals.org/doi/full/10.1161/CIR.0000000000000259

An important aspect of this topic is related to torsades de pointes, and its prediction and prevention. A number of ECG predictors of imminent risk of sustained torsades de pointes have been reported. Patients with any of these ECG findings deserve urgent attention. These include:

1. Bursts of nonsustained polymorphic ventricular tachycardia in the setting of QT(U) prolongation
2. Marked QT prolongation
3. Large U waves with a long QT(U)
4. QT or U wave alternans
5. Ventricular bigeminy, especially for sustained periods in patients with a long QT(U). The “R on T” or “R on U” sign may be present, associated with “short-coupled” PVCs. These very early cycle PVCs, in turn, may be the surface ECG manifestation of early afterdepolarizations occurring at the cellular level because of membrane instability.
6. QT prolongation, especially with PVCs, in concert with second- or third-degree AV block

An example of an ECG heralding sustained torsades de pointes is shown in Fig. S2.9.

Fig. S2.9 ECG shows underlying sinus rhythm with an extremely long QT(U) (about 600 msec) due to the drug dofetilide, used chemically (pharmacologically) to cardiovert atrial fibrillation. Note the nonsustained runs of torsades de pointes. The extreme right axis deviation here is because of right–left arm limb lead reversal. Given these repolarization findings, the patient is in one of the highest risk groups to develop sustained torsades de pointes and cardiac arrest.
For additional information on prevention of torsades in the hospital setting, readers are referred to the AHA and other official cardiology society scientific statements and their updates: https://www.ahajournals.org/doi/10.1161/circulationaha.109.192704

Selected References
(1) Shimizu, W., & Antzelevitch, C. (1999). Cellular and ionic basis for T-wave alternans under long-QT conditions. Circulation, 99, 1499–1507.
(2) Lerma, C., Lee, C. F., Glass, L., et al. (2007). The rule of bigeminy revisited: Analysis in sudden cardiac death syndrome. J Electrocardiol, 40, 78–88.

Supplement to Chapter 22: Pacemakers and ICDs

The American College of Cardiology, the American Heart Association, and the Heart Rhythm Society publish updated Guidelines for Device-based Therapy of Cardiac Rhythm Abnormalities. These guidelines are available at the various societies’ website including,

http://content.onlinejacc.org/article.aspx?articleid=1357576

Chest X-Ray with Electronic Devices
Fig. S2.10 shows chest radiographs from two patients: one with a pacemaker and one with an implantable cardioverter–defibrillator (ICD). See caption for details.

Fig. S2.10 (A) Chest X-ray from a patient with a dual-chamber pacemaker (PM). The generator is in the left pectoral area and the leads (electrodes) are positioned in the right atrium and right ventricular (RV) apex. (B) Chest X-ray from a patient with an implantable cardioverter–defibrillator (ICD) with biventricular pacing leads. Note the larger size of the ICD generator compared to the pacemaker in (A). The RV lead has two high-voltage coils (thick components), which are used to deliver shocks. The left ventricular (LV) lead goes through the lateral branch of the coronary sinus to the LV lateral wall. Note the absence of a right atrial lead: this patient had chronic (permanent) atrial fibrillation, precluding the need for atrial pacing.

Post-Pacemaker T Wave Inversions: Cardiac Memory and the Differential Diagnosis of Precordial T Wave Inversions
Ventricular pacing markedly changes the activation pattern of the ventricles, resulting in a wide QRS complex with discordant T waves, that is, the T wave vector typically is oriented in a direction opposite to that of the main QRS vector. A similar discordance of QRS and T wave vectors is seen with the secondary T wave changes associated with bundle branch blocks or with premature ventricular complexes (see Chapters 8 and 16).
Of importance (and less well recognized) is the finding that ventricular pacing also may produce changes in repolarization after ventricular pacing has stopped and normal QRS activation has resumed. These changes, referred to as post-pacing or post-pacemaker T wave inversions, are the most common manifestation of so-called cardiac memory T waves.
Cardiac memory is the general term used to refer to T wave inversions that appear upon resumption of normal ventricular depolarization after a period of abnormal activation associated with electronic ventricular pacing, intermittent left bundle branch block, intermittent Wolff–Parkinson–White pattern, or prolonged ventricular tachycardia.
The principal feature (and reason for the unusual term “cardiac memory”) is the surprising observation that T wave polarity after ventricular pacing (when the QRS may be of normal duration) follows the direction (“remembers”) the QRS polarity during ventricular pacing. Right ventricular pacing typically produces a QRS with a left bundle branch block (LBBB) morphology, along with left axis deviation (Fig. S2.10). Thus, the ECG shows negative QRS complexes in the right to mid-precordial leads and positive QRS complexes in leads I and aVL. With intermittent or prior right ventricular pacing of sufficient duration, the T waves in normally conducted beats often show “memory” T waves manifest by T waves that are inverted (negative) in the right-mid precordial leads but positive in leads I and aVL. The basic mechanisms for memory T waves, a finding noted for decades, remain under active investigation.
Clinicians should be aware of this pattern since cardiac memory T wave inversions may confound the diagnosis of myocardial ischemia. Indeed, the post-pacemaker T wave pattern closely resembles that seen in Wellens’ syndrome (LAD-T wave inversion pattern) (see Chapters 9 and 21). Both conditions—ischemia and post-pacemaker depolarization—are characterized by prominent T wave inversions in the precordial leads. Given their similarities, patients with pacemakers may undergo unnecessary cardiac catheterization and coronary angiography because of anterior precordial T wave inversions that are mistaken as evidence of ischemia.
A key point of distinction is that most but not all patients with the LAD-T wave pattern (Wellens’ syndrome) have T wave inversions in multiple precordial leads and in leads aVL and/or I. Post-pacemaker (right ventricular) T wave inversions can only account for T wave inversions in precordial leads, not in leads I and aVL, where upright T waves are found. Therefore, T wave inversions in leads I, aVL, and in multiple precordial leads cannot be attributed to intermittent or prior right ventricular pacing (or to intermittent LBBB). Furthermore, post-pacemaker T wave inversions are also usually associated with T wave inversions in the inferior limb and precordial leads, in contrast to LAD-T wave inversions (Fig. S2.11).

Fig. S2.11 (A) T wave inversions due to transient left anterior descending (LAD) ischemia/occlusion (often referred to as Wellens’ syndrome). Note the deep precordial (chest lead) T wave inversions in concert with T wave inversions in leads I and aVL. However, in some cases of Wellens’ syndrome, T wave inversions may not appear in leads I and aVL. (B) Post-pacemaker (memory) T wave changes. This ECG was obtained after sustained pacing of the right ventricle. The normally conducted beats now show T wave inversions, simulating ischemia. Note, however, that leads I and aVL show positive T waves, in contrast to the classic Wellens’ (LAD-T wave inversion) pattern shown in panel (A).

For further information on this more advanced topic, interested readers are referred to the references below.

Selected References
(1) Rosenbaum, M.B., Blanco, H. H., Elizari, M. V., et al. (1982). Electrotonic modulation of the T wave and cardiac memory. Am J Cardiol, 50, 213–222.
(2) de Zwaan, C., Bar, F. W., & Wellens, H. J. (1982). Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J, 103, 730–736.
(3) de Zwaan, C., Bar, F. W., Janssen, J. H., et al. (1989). Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. Am Heart J, 117, 657–665.
(4) Shvilkin, A., Ho, K. K., Rosen, M. R., et al. (2005). T-vector direction differentiates postpacing from ischemic T-wave inversion in precordial leads. Circulation, 111, 969–974.
(5) Byrne, R., & Filippone, L. (2010). Benign persistent T-wave inversion mimicking ischemia after left bundle-branch block—cardiac memory. Am J Emerg Med, 28:e745-7.
(6) Shvilkin, A., Huang, H. D., & Josephson, M. E. (2015). Cardiac memory: diagnostic tool in the making. Circ Arrhythm Electrophysiol, 8, 2475–2482.

Pacemakers and Implantable Cardioverter–Defibrillators: Frequently Asked Questions (FAQs) by Patients and Primary Caregivers
Patients with permanent pacemakers (PPMs) and implantable cardioverter–defibrillators (ICDs), collectively referred to as cardiac implantable electronic devices (CIEDs), often ask primary caregivers questions about these devices. The material here provides some general answers to frequently asked questions (FAQs) that may be helpful while your patients are awaiting follow-up with their cardiologist. This material may also help guide clinicians in speaking with the specialist who monitors their device. CIED features become more and more complex with wide variations between device types, models, and manufacturers. Therefore, specific device issues should be discussed with an EP specialist.
Q: How do I know that my pacemaker/ICD is working?
A: PPMs and ICDs are reliable devices and malfunctions are exceedingly uncommon. However, your cardiologist must check these devices regularly. Traditionally this noninvasive procedure (called “device interrogation”) is performed in the doctor’s office. The PPM or ICD interfaces with a programming unit. All of the important data about your device (e.g., battery longevity, arrhythmia detections, lead integrity) will be reviewed. Additionally, any reprogramming changes can be made during the in-office interrogation. The majority of the newer devices are capable of remote monitoring through a stand-alone “home monitor” or a smartphone app. In addition to the daily automatic checks, you can manually transmit data recorded by your device to a physician or electrophysiology technician. Many ICDs have an audible alarm that will alert the patient about problems such as low battery, lead malfunction, or certain serious arrhythmias. If you hear these alarms, contact your cardiologist immediately. You should discuss with your cardiologist the plan for your device monitoring.
Q: How long is my battery going to last?
A: Battery longevity varies depending on the type of the device and its use. Most PPM batteries last at least 10 years; ICD batteries last 7 to 10 years. The longevity of cardiac resynchronization devices (CRTs/biventricular pacemakers) is slightly shorter. Fortunately, the PPM and ICD batteries do not cease to function suddenly. Instead, they are designed to provide ample warning time (3 months or longer) before the battery completely runs out and they automatically switch to a power-saving backup mode. Furthermore, the effectiveness of the device does not decrease with aging of the battery.
Q: Will I feel it if my ICD goes off (discharges)?
A: Most likely, yes. However, sensitivity to shocks varies greatly among patients. Surprisingly, some patients do not feel shocks at all. An ICD shock may not be felt if it happens during sleep or if the patient has already fainted (experienced syncope) from the arrhythmia.
Q: What do I do if I think my device “went off?”
A: Only ICDs can deliver electrical shocks to the heart; pacemakers do not. If you have had shocks before that were evaluated by your doctor but feel perfectly normal before and after the shock, you can call your cardiologist for an appointment the same or the next day or (if your device supports remote follow-up) send a remote rhythm transmission for evaluation.
Call 911 if you experience any of the following!

• First shock ever
• ANY unusual symptoms either before or after the shock (especially chest discomfort, shortness of breath, dizziness, or palpitations)
• More than one shock delivered

Also, call your cardiologist/EP specialist urgently if you learn that your ICD has a “recalled” (failure-prone) lead or if you feel concerned for any other reason.
Q: Is my device (PPM, ICD) safe around the microwave, TV, phone, etc.?
A: Yes, there is no risk of interference with usual household appliances. However, large industrial electrical motors and appliances producing strong electromagnetic fields (e.g., arc welders) should be avoided. Do not keep your cell phone in the shirt pocket on the side of the device.
Q: What happens if I accidentally walk through an airport metal detector or anti-theft device at a store?
A: There is negligible, if any, risk of metal detector interference with the proper device functioning. Since screening procedures at the airports are constantly changing, the safest way is to inform the security personnel about the implantable device and follow their instructions. Anti-theft gates at department stores can produce a magnet effect and should be transited quickly.
Q: If my ICD goes off during sexual intercourse will my partner feel it?
A: Yes, most likely they will. However, the transmitted sensation is not life-threatening.
Q: I have a hybrid/electric car. Will its motor and smart key affect my device?
A: Hybrid and electric car motors are considered safe for the devices as long as you do not get too close to the engine. (Do not be your own mechanic!) Smart keys do not interfere with PPMs/ICDs.
Q: When can I drive after ICD implantation?
A: For ICDs implanted for primary arrhythmia prevention (i.e., prophylaxis in high-risk patients without prior syncope or sudden cardiac arrest because of spontaneous sustained ventricular tachyarrhythmia), no driving for 1 week is recommended. For ICDs implanted for secondary prevention (i.e., survivors of a cardiac arrest caused by ventricular fibrillation or hemodynamically unstable, sustained ventricular tachycardia), no driving for 6 months after the episode of ventricular arrhythmia leading to device implantation (and subsequent episodes causing device shocks) is mandatory (enforced by state laws). Note: Commercial licensing is subject to federal law, according to which an ICD for any reason currently makes a person ineligible for certification.
Q: Can I have a computerized tomography (CT) or magnetic resonance imaging (MRI) scan with my PPM/ICD?
A: CT scans are safe for all patients with PPMs/ICDs. Historically, MRIs have been contraindicated in patients with CIEDs. However, the latest models of CIEDs are labeled “MRI -conditional” meaning they are safe for MRI tests under specified conditions. Despite this designation, there are certain restrictions and precautions that must be followed for their safe use and most of them need to be reprogrammed in a special “MRI-safe” mode before and after the test. Importantly, these devices can be used only in conjunction with “MRI-safe” leads and will not work with the older non-MRI-compliant leads. Recently, MRI scans with older (so-called legacy) device models are being performed—shared decision-making with patients, electrophysiologists, and radiologists is of paramount importance for performing MRIs when older CIEDs are in place.
Therapeutic radiation (for the treatment of malignancies) of the CIED field can produce unpredictable damage to the device if a certain dose threshold is exceeded. The device should be shielded or even explanted if necessary. Radiation and EP specialists together with determine the appropriate course of action. Remote device monitoring helps detect device malfunctions in real time.
Q: Does implanting a PPM/ICD require open-heart surgery?
A: No. In general, implanting a PPM or ICD involves inserting the lead(s) into the heart chambers through a vein in the upper chest wall, and attaching it/them to the battery, secured in a “pocket” made after a small incision underneath the clavicle. The procedure is done with local anesthesia and often with conscious sedation (similar to the anesthesia done for colonoscopies). After the procedure, you will be instructed about wound care, follow-up, and short-term arm restrictions. Many patients are discharged from the hospital the same day after the procedure.
Q: I have an ICD. Do I need a PPM as well?
A: No. All current transvenous ICDs function as pacemakers.
Q: I have heard about subcutaneous (SubQ) ICDs. What is the difference between SubQ and traditional ICDs?
A: Subcutaneous ICDs have no wires going through the veins or attached to the heart. The ICD canister (“can”), consisting of the mini-computer with the battery, is implanted under the left axilla and the defibrillation lead is placed under the skin to the left of the sternum. This placement reduces the risk of blood-born infections associated with intracardiac device wires and makes it easier and safer to replace the wire in case of malfunction. The effectiveness of the subcutaneous device is similar to that of a traditional ICD. The only exception is that the subcutaneous ICD cannot function as a pacemaker.
Q: My patient says they have a pacemaker but there are no scars or palpable device on the chest. How can that be?
A: The patient likely has a leadless pacemaker, which is a bullet-sized/shaped device implanted directly into the heart usually through the femoral vein. There are no wires attached and no incisions required. Leadless pacemakers can be located with the device programmer (or seen on the chest X-ray).
Q: I hear a lot about “physiologic pacing.” What is it?
A: “Physiologic pacing” or “conduction system pacing”(including “His bundle pacing” and “left bundle branch area pacing”) is the technique of engaging the viable portions of the native conduction system to activate the ventricles in a synchronous way. The ventricular electrode is placed in contact with either the His bundle or the left bundle branch area instead of the right ventricular muscle. Physiologic pacing produces a narrow QRS and provides cardiac resynchronization. In many cases it can be used instead of traditional cardiac resynchronization (biventricular pacing) therapy (CRT).
Q: The patient’s automatic (computer-generated) ECG interpretation says “AV paced rhythm” but I do not see any pacing spikes and the QRS complex looks narrow. Is there pacemaker malfunction?
A: Low output or short duration pacing stimuli can be detected by the ECG machine but might not be visible (especially at usual gain) on the surface ECG recording. Ventricular pacing with a relatively narrow (normal duration) QRS can be a result of pseudo-fusion (ventricular activation through normal conduction system occurring nearly simultaneous with the pacing spike) or conduction system (physiologic) pacing.

Chapter 23: Interpreting ECGs: an Integrative Approach

As discussed in this chapter and emphasized throughout the text, a systematic approach to ECG analysis is essential. ECG reading errors are surprisingly common. They can be grouped into two major categories:

1. Errors of commission (“type I” errors or false positives)
2. Errors of omission (“type II” errors or false negatives)

An example of the first category would be mistaking the ST elevations of benign early repolarization, Brugada pattern, or stable left bundle branch block for an acute ST segment elevation MI (STEMI), and initiating inappropriate emergency cardiac catheterization and antithrombotic therapy. An example of the latter is failing to identify AF in a patient with heart failure (e.g., reading the rhythm as sinus with premature atrial complexes and not anticoagulating a patient).
There are many reasons why even experienced medical professionals make errors in general and ECG reading errors in particular. Misinterpretations of ECGs have at least four major causes:

• Haste/time pressures: Looking but not seeing
• Cognitive lacunae: Seeing but not knowing
• Reliance on computers: Looking but not thinking
• “Ruse for real:” Mistaking artifact for actual

AF is a very important source of mistakes, subject to both missed detections and overdiagnosis. In one still relevant, retrospective study1 from a community hospital, 2,809 cases of AF were identified by expert consensus re-review from a total of 35,508 ECGs performed over a given time period. Incorrect diagnoses related to AF were found in 219 of the reviewed cases. Type I errors (overdiagnosis) occurred in 137 cases (8%). False-positive errors were related to rhythms with irregular RR intervals (e.g., sinus rhythm with premature atrial complexes and atrial tachycardia or atrial flutter with variable AV conduction) being mistaken for AF. The presence of low-amplitude atrial activity or baseline artifact significantly increased the likelihood of this type of error. Type II errors (missed AF) occurred in 82 cases of actual AF (3%) where the arrhythmia was either completely missed or confused with atrial tachycardia/flutter. Of particular note, electronic ventricular pacing significantly increased the likelihood of missing underlying AF in this study because of regularization of the ventricular response.
Recall also that computerized (electronic) ECG interpretations may lead to false-positive and false-negative readings in AF and other arrhythmias.2 As emphasized in the text, computerized interpretations must always be carefully read over by ECG professionals.
In a more recent meta-analysis3 of 78 original studies, the accuracy of ECG interpretation was low in the absence of physician training, varying widely across studies. Accuracy improved after training but was disappointing still low. Further improvements were noted with progressive training and specialization, emphasizing the need for ongoing training, reinforcement, and assessment in this vital area of clinical skills.

References
(1) Davidenko, J. M., & Snyder, L. S. (2007). Causes of errors in the electrocardiographic diagnosis of atrial fibrillation by physicians. J Electrocardiol, 40, 450–456.
(2) Bae, M. H., et al. (2012). Erroneous computer ECG interpretation of atrial fibrillation and its clinical consequences. Clin Cardiol, 35, 348–353.
(3) Cook, D. A., Oh, S. Y., & Pusic, M. V. (2020). Accuracy of physicians’ electrocardiogram interpretations: A systematic review and meta-analysis. JAMA Intern Med, 180, 1–11.